causes of hiv essay

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Cause and Risk Factors of HIV

• Sex Risk Factors

Injecting Drug Use

Needlestick injuries, blood transfusions, frequently asked questions.

• Next in HIV/AIDS Guide What Tests Can Diagnose HIV?

This article is part of  Health Divide: HIV , a destination in our Health Divide series.

HIV (human immunodeficiency virus) is a virus that can be passed from one person to the next through body fluids like semen, blood, vaginal secretions, and breast milk. HIV is most often transmitted during sex but can also be passed through  shared needles . HIV can also be transmitted from the carrying parent to child during pregnancy, childbirth, or while  breastfeeding .

Unlikely routes of transmission include blood transfusions, tattooing, and body piercing.

Other factors can increase the risk of transmission. Some of which are specific to certain groups because social factors, like discrimination and stigma , uniquely position them to be more likely to test HIV positive. These groups include Black people, Latinx people, trans people (especially trans women), men who have sex with men (MSM) , and injecting drug users.

HIV is a type of virus known as a retrovirus. It works by targeting immune cells called CD4 T cells that are responsible for instigating the immune response. When one of these cells is infected, the virus will "hijack" its genetic machinery and turn it into an HIV-producing factory. As the infected cell dies, the newly emergent viruses will go on to infect other CD4 T cells.

By progressively targeting and killing these cells, the body becomes less and less able to fight infections that it would otherwise be able to defend itself against.

When the immune defenses are compromised, serious and potentially life-threatening opportunistic infections can develop. This is the stage of infection commonly known as AIDS (acquired immune deficiency syndrome) .

Even though HIV is transmitted through body fluids, not all body fluids are capable of transmitting the virus. Some fluids like saliva and urine contain high levels of enzymes or acids that prevent HIV from thriving. Once outside of the body, the virus is unable to survive for very long (and usually not at levels where transmission is likely).

Moreover, the virus must come in contact with mucosal tissues (such as found in the rectum or vagina) or enter the body through broken skin—and in sufficient quantities—to establish an infection.

Vaginal fluids

Rectal secretions

Breast milk

Shared utensils

Toilet seats

Pool or bath water

Mosquito bites

Sexual Risk Factors

The risk of HIV from sex varies by the type of sexual activity and other factors. The risk is greatest when condoms are not used. And, while it is possible not to get HIV after a single act of unprotected sex, people have gotten HIV after just one exposure.

According to the Centers for Disease Control and Prevention (CDC), the per-act risk of HIV from sex is as follows:

• Receptive anal sex : 138 per 10,000 exposures (1.38%)
• Insertive anal sex: 11 per 10,000 exposures (0.11%)
• Receptive vaginal sex : 8 per 10,000 exposures (0.08%)
• Insertive vaginal sex: 4 per 10,000 exposures (0.04%)
• Oral sex : Risk is low to negligible

Additional Risk Factors

These per-act statistics may make it seem as if your general risk of HIV is extremely low, but they don't paint the complete picture. Other risk factors can amplify the risk, sometimes dramatically.

Among the risk factors to consider:

• Anal sex : Anal sex is one of the most effective routes of transmission because rectal tissues are delicate and easily broken. Unlike the vagina, the rectal canal only has a single layer of cells overlying tissues that are rich in CD4 T cells.
• Receptive sex : People with vaginas are more likely to get HIV from vaginal sex in part because the area of vulnerable tissues in the vagina is larger than those in the male urethra . The same applies to people who engage in receptive ("bottom") anal sex who are more likely to get HIV than their insertive ("top") partner.
• HIV viral load : The HIV viral load is a test used to measure the amount of HIV in your blood, which can range from undetectable to well over a million. Not surprisingly, having a high viral load increases the risk of transmission, while a low viral load decreases the risk.
• Sexually transmitted infections (STIs) : STIs commonly occur with HIV and can facilitate infection in different ways. Certain STIs like syphilis cause ulcers that provide HIV easy access into the body. STIs also trigger an inflammatory response that draws immune cells to the site of the infection, providing more CD4 T cells for the virus to target and hijack.
• Multiple partners : “Statistically, the more sexual partners you have, the greater opportunity there is to test positive for HIV. Moreover, a large sexual network can expose you to different drug-resistant HIV strains that may not respond as well to HIV medications.
• Spermicides : Nonoxynol-9 , a spermicide used to prevent pregnancy, can be irritating and trigger an inflammatory response that draws immune cells closer to the surface of the vagina. The Food and Drug Administration (FDA) currently advises against the use of nonoxynol-9 if a sexual partner has HIV.
• Douching : Vaginal and anal douching strips tissues of mucus that provide some protection against HIV. There is debate as to how much this can increase a person's risk of infection, but the current evidence suggests that anal douching is potentially concerning.

The sharing of needles, syringes, and other drug paraphernalia is an effective way to pass HIV from one person to the next. The transmission of the virus is especially high when a person has a high viral load. Other practices such as "booting" or "kicking" (in which blood is drawn into the syringe and then injected) further amplify the risk.

According to the CDC, the risk of HIV from sharing needles is 63 per 10,000 exposures (0.63%). In certain countries, like Russia, injecting drug use is the predominant mode of HIV transmission, not sex.

Even beyond exposure to HIV-contaminated blood, people who are under the influence of drugs are more likely to engage in risky sexual behaviors, including unprotected sex, sex with multiple partners, or trading sex for money or drugs.

Since the 1990s, clean needle exchange programs have successfully reduced the rate of HIV and other communicable diseases such as hepatitis C by distributing clean syringes to drug users.

HIV and Injecting Drug Use in MSM and Trans Women

Men who have sex with men (MSM) are more than twice as likely to inject drugs than other men, most of whom are white and under age 35. Trans women and other transfeminine people are also more likely to use injection drugs compared to the general population. The drug methamphetamine is especially troubling as it increases the risk of HIV by 50% compared to other injected drugs (due in part to the hypersexual behaviors it can arouse).

Pregnancy and Breastfeeding

Pregnancy is a less common mode of infection but one that still poses risks to certain groups. There are three circumstances under which a birthing parent with HIV can pass the virus to their baby: during pregnancy, delivery, breastfeeding, or chestfeeding (feeding a baby milk from your chest).

The transmission of the virus before or during childbirth is largely the result of the rupture of the placenta which exposes the baby to HIV-positive blood. HIV is also present in chest milk or breast milk and can potentially cause infection, particularly if the birthing parent does not have an undetectable viral load.

In the United States, birthing parent-to-child transmission of HIV is rare, thanks to routine prenatal screening and the use of antiretroviral drugs which can reduce the risk of transmission to less than 1%. Even if a birthing parent arrives at the hospital with no prior prenatal care, an intravenous infusion of antiretroviral drugs used in combination with a cesarean section can greatly reduce the risk of transmission.

In the United States, parents are advised not to breastfeed if they have HIV and to bottle-feed instead. In developing countries, the benefits of exclusive breastfeeding (in terms of nutrition and the building of immunity) are seen to outweigh the risks in resource-poor communities.

In 2014, only 33 reported cases of birthing parent-to-child transmission of HIV were reported in the United States.

Pregnancy Risks Among Black Women With HIV

Despite the low number of mother-to-child transmissions in the United States, the risk among Black women is eight times greater than in White women and seven times greater than in Latinx women. Moreover, 60% of children living with HIV are born to Black mothers with HIV.

Needlestick injuries (sometimes referred to as sharps injuries) can expose a person to tainted blood or body fluids. The risk is of concern for doctors, nurses, and other healthcare workers who are vulnerable to blood-borne infections from patients.

Even so, the CDC suggests that the risk is low due to universal precautions that are designed to reduce the risk of disease transmission to healthcare workers. Today, the per-incidence risk of HIV from a needlestick injury is roughly 0.23%.

If an accident does occur, a preventive strategy called post-exposure prophylaxis (PEP) may avert an infection if started within 72 hours of the exposure. PEP involves a 28-day course of antiretroviral drugs and may reduce the likelihood of HIV from a high-risk exposure by 81%.

In the early days of the AIDS pandemic, a blood transfusion was a common cause of HIV infection. With the institution of HIV blood screening in 1985 and universal blood screening in 1992, the likelihood of transmission by this route is almost unheard of.

In fact, according to the CDC, there were only three confirmed cases of HIV out of an estimated 2.5 million blood transfusions from 1999 to 2013.

Similarly, state regulations governing the licensing of tattoo and piercing parlors have also made these procedures unlikely causes of HIV. To date, there are no documented cases of HIV transmission from either tattooing or body piercing . The CDC considers the risk negligible.

A Word From Verywell

Understanding the causes and risk factors of HIV can help you develop strategies to protect yourself whether you have HIV or don't. This first step is getting diagnosed and knowing your HIV status.

If you don't have HIV, you can avoid infection by using condoms, reducing your number of sex partners, or using a preventive strategy called pre-exposure prophylaxis (PrEP) , which can reduce your risk of HIV by as much as 99%.

If you have HIV, early treatment can cut your risk of serious HIV- and non-HIV-related illness by more than half while allowing you to enjoy a normal to near-normal life expectancy . Moreover, having an undetectable viral load reduces your risk of infecting others to zero .

HIV stands for the human immunodeficiency virus. The virus causes disease by targeting and killing immune cells, called CD4 T-cells , that are responsible for coordinating the immune defense. As these cells are progressively destroyed, the body becomes less and less able to defend itself against infections that it could otherwise control.

"AIDS" is the term used to describe the stage in which the immune system is compromised by HIV infection. Traditionally, AIDS is diagnosed when the CD4 count falls below 200 or when you get any one of the 29 different diseases classified as AIDS-defining conditions .

Most people get HIV through sex, namely vaginal or anal sex. HIV can also be passed through shared needles or needlestick injuries in healthcare settings. Mothers with HIV can pass the virus to their babies during pregnancy (although this is less common in the United States due to the routine testing and treatment of mothers during perinatal care).

You cannot get HIV from kissing, touching, hugging, toilet seats, shared utensils, or mosquito bites. In the past, there was a risk of getting HIV from a blood transfusion, but this rarely occurs in the United States due to routine blood screening. Tattooing and piercing can theoretically transmit HIV, but there has yet to be a documented case of this occurring in the United States.

The risk of getting HIV is higher for:

• People who engage in sex without condoms
• People with multiple sex partners
• Injecting drug users who share needles
• Black and Latinx people
• Trans people, especially trans women
• Men who have sex with men (MSM)
• Having sex with someone who shares needles or has multiple sex partners
• Having another sexually transmitted infection (STI)

Theoretically, you can, but there are few documented cases of this occurring. This is partly because the environment in the mouth is hostile to the virus and the tissues of the mouth aren't as susceptible as some other areas of the body. Even so, other STIs can be passed through oral sex, but they may be avoided with condoms or dental dams .

There are multiple factors that contribute to this. Transphobia, homophobia, and HIV stigma contribute to high rates of denial, secrecy, and depression. This, in turn, increases the risk of substance or alcohol abuse and risk-taking behaviors. Black people also experience higher rates of criminalization and homelessness in comparison to the general population. These factors are additive and result in a higher likelihood of testing positive for HIV in one’s lifetime. The extreme vulnerability of rectal tissues and smaller gay and trans sexual networks due to the reasons stated above also contribute.

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By Mark Cichocki, RN Mark Cichocki, RN, is an HIV/AIDS nurse educator at the University of Michigan Health System for more than 20 years.  

• Patient Care & Health Information
• Diseases & Conditions

Acquired immunodeficiency syndrome (AIDS), is an ongoing, also called chronic, condition. It's caused by the human immunodeficiency virus, also called HIV. HIV damages the immune system so that the body is less able to fight infection and disease. If HIV isn't treated, it can take years before it weakens the immune system enough to become AIDS . Thanks to treatment, most people in the U.S. don't get AIDS .

HIV is spread through contact with genitals, such as during sex without a condom. This type of infection is called a sexually transmitted infection, also called an STI. HIV also is spread through contact with blood, such as when people share needles or syringes. It is also possible for a person with untreated HIV to spread the virus to a child during pregnancy, childbirth or breastfeeding.

There's no cure for HIV / AIDS . But medicines can control the infection and keep the disease from getting worse. Antiviral treatments for HIV have reduced AIDS deaths around the world. There's an ongoing effort to make ways to prevent and treat HIV / AIDS more available in resource-poor countries.

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The symptoms of HIV and AIDS vary depending on the person and the phase of infection.

Primary infection, also called acute HIV

Some people infected by HIV get a flu-like illness within 2 to 4 weeks after the virus enters the body. This stage may last a few days to several weeks. Some people have no symptoms during this stage.

Possible symptoms include:

• Muscle aches and joint pain.
• Sore throat and painful mouth sores.
• Swollen lymph glands, also called nodes, mainly on the neck.
• Weight loss.
• Night sweats.

These symptoms can be so mild that you might not notice them. However, the amount of virus in your bloodstream, called viral load, is high at this time. As a result, the infection spreads to others more easily during primary infection than during the next stage.

Clinical latent infection, also called chronic HIV

In this stage of infection, HIV is still in the body and cells of the immune system, called white blood cells. But during this time, many people don't have symptoms or the infections that HIV can cause.

This stage can last for many years for people who aren't getting antiretroviral therapy, also called ART. Some people get more-severe disease much sooner.

Symptomatic HIV infection

As the virus continues to multiply and destroy immune cells, you may get mild infections or long-term symptoms such as:

• Swollen lymph glands, which are often one of the first symptoms of HIV infection.
• Oral yeast infection, also called thrush.
• Shingles, also called herpes zoster.

Progression to AIDS

Better antiviral treatments have greatly decreased deaths from AIDS worldwide. Thanks to these lifesaving treatments, most people with HIV in the U.S. today don't get AIDS . Untreated, HIV most often turns into AIDS in about 8 to 10 years.

Having AIDS means your immune system is very damaged. People with AIDS are more likely to develop diseases they wouldn't get if they had healthy immune systems. These are called opportunistic infections or opportunistic cancers. Some people get opportunistic infections during the acute stage of the disease.

The symptoms of some of these infections may include:

• Fever that keeps coming back.
• Ongoing diarrhea.
• Swollen lymph glands.
• Constant white spots or lesions on the tongue or in the mouth.
• Constant fatigue.
• Rapid weight loss.
• Skin rashes or bumps.

When to see a doctor

If you think you may have been infected with HIV or are at risk of contracting the virus, see a healthcare professional as soon as you can.

More Information

• Early HIV symptoms: What are they?

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HIV is caused by a virus. It can spread through sexual contact, shooting of illicit drugs or use of shared needles, and contact with infected blood. It also can spread from parent to child during pregnancy, childbirth or breastfeeding.

HIV destroys white blood cells called CD4 T cells. These cells play a large role in helping the body fight disease. The fewer CD4 T cells you have, the weaker your immune system becomes.

How does HIV become AIDS?

You can have an HIV infection with few or no symptoms for years before it turns into AIDS . AIDS is diagnosed when the CD4 T cell count falls below 200 or you have a complication you get only if you have AIDS , such as a serious infection or cancer.

How HIV spreads

You can get infected with HIV if infected blood, semen or fluids from a vagina enter your body. This can happen when you:

• Have sex. You may become infected if you have vaginal or anal sex with an infected partner. Oral sex carries less risk. The virus can enter your body through mouth sores or small tears that can happen in the rectum or vagina during sex.
• Share needles to inject illicit drugs. Sharing needles and syringes that have been infected puts you at high risk of HIV and other infectious diseases, such as hepatitis.
• Have a blood transfusion. Sometimes the virus may be transmitted through blood from a donor. Hospitals and blood banks screen the blood supply for HIV . So this risk is small in places where these precautions are taken. The risk may be higher in resource-poor countries that are not able to screen all donated blood.
• Have a pregnancy, give birth or breastfeed. Pregnant people who have HIV can pass the virus to their babies. People who are HIV positive and get treatment for the infection during pregnancy can greatly lower the risk to their babies.

How HIV doesn't spread

You can't become infected with HIV through casual contact. That means you can't catch HIV or get AIDS by hugging, kissing, dancing or shaking hands with someone who has the infection.

HIV isn't spread through air, water or insect bites. You can't get HIV by donating blood.

Risk factors

Anyone of any age, race, sex or sexual orientation can have HIV / AIDS . However, you're at greatest risk of HIV / AIDS if you:

• Have unprotected sex. Use a new latex or polyurethane condom every time you have sex. Anal sex is riskier than is vaginal sex. Your risk of HIV increases if you have more than one sexual partner.
• Have an STI . Many STIs cause open sores on the genitals. These sores allow HIV to enter the body.
• Inject illicit drugs. If you share needles and syringes, you can be exposed to infected blood.

Complications

HIV infection weakens your immune system. The infection makes you much more likely to get many infections and certain types of cancers.

Infections common to HIV/AIDS

• Pneumocystis pneumonia, also called PCP. This fungal infection can cause severe illness. It doesn't happen as often in the U.S. because of treatments for HIV / AIDS . But PCP is still the most common cause of pneumonia in people infected with HIV .
• Candidiasis, also called thrush. Candidiasis is a common HIV -related infection. It causes a thick, white coating on the mouth, tongue, esophagus or vagina.
• Tuberculosis, also called TB. TB is a common opportunistic infection linked to HIV . Worldwide, TB is a leading cause of death among people with AIDS . It's less common in the U.S. thanks to the wide use of HIV medicines.
• Cytomegalovirus. This common herpes virus is passed in body fluids such as saliva, blood, urine, semen and breast milk. A healthy immune system makes the virus inactive, but it stays in the body. If the immune system weakens, the virus becomes active, causing damage to the eyes, digestive system, lungs or other organs.
• Cryptococcal meningitis. Meningitis is swelling and irritation, called inflammation, of the membranes and fluid around the brain and spinal cord, called meninges. Cryptococcal meningitis is a common central nervous system infection linked to HIV . A fungus found in soil causes it.

Toxoplasmosis. This infection is caused by Toxoplasma gondii, a parasite spread primarily by cats. Infected cats pass the parasites in their stools. The parasites then can spread to other animals and humans.

Toxoplasmosis can cause heart disease. Seizures happen when it spreads to the brain. And it can be fatal.

Cancers common to HIV/AIDS

• Lymphoma. This cancer starts in the white blood cells. The most common early sign is painless swelling of the lymph nodes most often in the neck, armpit or groin.
• Kaposi sarcoma. This is a tumor of the blood vessel walls. Kaposi sarcoma most often appears as pink, red or purple sores called lesions on the skin and in the mouth in people with white skin. In people with Black or brown skin, the lesions may look dark brown or black. Kaposi sarcoma also can affect the internal organs, including the lungs and organs in the digestive system.
• Human papillomavirus (HPV)-related cancers. These are cancers caused by HPV infection. They include anal, oral and cervical cancers.

Other complications

• Wasting syndrome. Untreated HIV / AIDS can cause a great deal of weight loss. Diarrhea, weakness and fever often happen with the weight loss.
• Brain and nervous system, called neurological, complications. HIV can cause neurological symptoms such as confusion, forgetfulness, depression, anxiety and difficulty walking. HIV -associated neurological conditions can range from mild symptoms of behavior changes and reduced mental functioning to severe dementia causing weakness and not being able to function.
• Kidney disease. HIV -associated nephropathy (HIVAN) is swelling and irritation, called inflammation, of the tiny filters in the kidneys. These filters remove excess fluid and waste from the blood and pass them to the urine. Kidney disease most often affects Black and Hispanic people.
• Liver disease. Liver disease also is a major complication, mainly in people who also have hepatitis B or hepatitis C.

There's no vaccine to prevent HIV infection and no cure for HIV / AIDS . But you can protect yourself and others from infection.

To help prevent the spread of HIV :

Consider preexposure prophylaxis, also called PrEP. There are two PrEP medicines taken by mouth, also called oral, and one PrEP medicine given in the form of a shot, called injectable. The oral medicines are emtricitabine-tenofovir disoproxil fumarate (Truvada) and emtricitabine-tenofovir alafenamide fumarate (Descovy). The injectable medicine is called cabotegravir (Apretude). PrEP can reduce the risk of sexually transmitted HIV infection in people at very high risk.

PrEP can reduce the risk of getting HIV from sex by about 99% and from injecting drugs by at least 74%, according to the Centers for Disease Control and Prevention. Descovy hasn't been studied in people who have sex by having a penis put into their vaginas, called receptive vaginal sex.

Cabotegravir (Apretude) is the first U.S. Food and Drug Administration-approved PrEP that can be given as a shot to reduce the risk of sexually transmitted HIV infection in people at very high risk. A healthcare professional gives the shot. After two once-monthly shots, Apretude is given every two months. The shot is an option in place of a daily PrEP pill.

Your healthcare professional prescribes these medicines to prevent HIV only to people who don't already have HIV infection. You need an HIV test before you start taking any PrEP . You need to take the test every three months for the pills or before each shot for as long as you take PrEP .

You need to take the pills every day or closely follow the shot schedule. You still need to practice safe sex to protect against other STIs . If you have hepatitis B, you should see an infectious disease or liver specialist before beginning PrEP therapy.

Use treatment as prevention, also called TasP. If you have HIV , taking HIV medicines can keep your partner from getting infected with the virus. If your blood tests show no virus, that means your viral load can't be detected. Then you won't transmit the virus to anyone else through sex.

If you use TasP , you must take your medicines exactly as prescribed and get regular checkups.

• Use post-exposure prophylaxis, also called PEP, if you've been exposed to HIV . If you think you've been exposed through sex, through needles or in the workplace, contact your healthcare professional or go to an emergency room. Taking PEP as soon as you can within the first 72 hours can greatly reduce your risk of getting HIV . You need to take the medicine for 28 days.

Use a new condom every time you have anal or vaginal sex. Both male and female condoms are available. If you use a lubricant, make sure it's water based. Oil-based lubricants can weaken condoms and cause them to break.

During oral sex, use a cut-open condom or a piece of medical-grade latex called a dental dam without a lubricant.

• Tell your sexual partners you have HIV . It's important to tell all your current and past sexual partners that you're HIV positive. They need to be tested.
• Use clean needles. If you use needles to inject illicit drugs, make sure the needles are sterile. Don't share them. Use needle-exchange programs in your community. Seek help for your drug use.
• If you're pregnant, get medical care right away. You can pass HIV to your baby. But if you get treatment during pregnancy, you can lessen your baby's risk greatly.
• Consider male circumcision. Studies show that removing the foreskin from the penis, called circumcision, can help reduce the risk of getting HIV infection.
• About HIV and AIDS . HIV.gov. https://www.hiv.gov/hiv-basics/overview/about-hiv-and-aids/what-are-hiv-and-aids. Accessed Oct. 18, 2023.
• Sax PE. Acute and early HIV infection: Clinical manifestations and diagnosis. https://www.uptodate.com/contents/search. Accessed Oct. 18, 2023.
• Ferri FF. Human immunodeficiency virus. In: Ferri's Clinical Advisor 2024. Elsevier; 2024. https://www.clinicalkey.com. Accessed Oct. 18, 2023.
• Guidelines for the prevention and treatment of opportunistic infections in adults and adolescents with HIV . HIV.gov. https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-opportunistic-infections/immunizations. Accessed Oct. 18, 2023.
• AskMayoExpert. Human immunodeficiency virus (HIV) infection. Mayo Clinic; 2023.
• Elsevier Point of Care. Clinical Overview: HIV infection and AIDS in adults. https://www.clinicalkey.com. Accessed Oct. 18, 2023.
• Male circumcision for HIV prevention fact sheet. Centers for Disease Control and Prevention. https://www.cdc.gov/nchhstp/newsroom/fact-sheets/hiv/male-circumcision-HIV-prevention-factsheet.html. Accessed Oct. 19, 2023.
• Acetyl-L-carnitine. Natural Medicines. https://naturalmedicines.therapeuticresearch.com. Accessed. Oct. 19, 2023.
• Whey protein. Natural Medicines. https://naturalmedicines.therapeuticresearch.com. Accessed. Oct. 19, 2023.
• Saccharomyces boulardii. Natural Medicines. https://naturalmedicines.therapeuticresearch.com. Accessed Oct. 19, 2023.
• Vitamin A. Natural Medicines. https://naturalmedicines.therapeuticresearch.com. Accessed Oct. 19, 2023.
• Red yeast rice. Natural Medicines. https://naturalmedicines.therapeuticresearch.com. Accessed Oct. 19, 2023.

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What Is HIV?

HIV ( human immunodeficiency virus ) is a virus that attacks cells that help the body fight infection, making a person more vulnerable to other infections and diseases. It is spread by contact with certain bodily fluids of a person with HIV, most commonly during unprotected sex (sex without a condom or HIV medicine to prevent or treat HIV), or through sharing injection drug equipment.

If left untreated, HIV can lead to the disease AIDS ( acquired immunodeficiency syndrome ).

The human body can’t get rid of HIV and no effective HIV cure exists. So, once you have HIV, you have it for life. Luckily, however, effective treatment with HIV medicine (called antiretroviral therapy or ART) is available. If taken as prescribed, HIV medicine can reduce the amount of HIV in the blood (also called the viral load) to a very low level. This is called viral suppression. If a person’s viral load is so low that a standard lab can’t detect it, this is called having an undetectable viral load. People with HIV who take HIV medicine as prescribed and get and keep an undetectable viral load can live long and healthy lives and will not transmit HIV to their HIV-negative partners through sex .

In addition, there are effective methods to prevent getting HIV through sex or drug use, including pre-exposure prophylaxis (PrEP) , medicine people at risk for HIV take to prevent getting HIV from sex or injection drug use, and post-exposure prophylaxis (PEP) , HIV medicine taken within 72 hours after a possible exposure to prevent the virus from taking hold. Learn about other ways to prevent getting or transmitting HIV .

What Is AIDS?

AIDS is the late stage of HIV infection that occurs when the body’s immune system is badly damaged because of the virus.

In the U.S., most people with HIV do not develop AIDS because taking HIV medicine as prescribed stops the progression of the disease.

A person with HIV is considered to have progressed to AIDS when:

• the number of their CD4 cells falls below 200 cells per cubic millimeter of blood (200 cells/mm3). (In someone with a healthy immune system, CD4 counts are between 500 and 1,600 cells/mm3.) OR
• they develop one or more opportunistic infections regardless of their CD4 count.

Without HIV medicine, people with AIDS typically survive about 3 years. Once someone has a dangerous opportunistic illness, life expectancy without treatment falls to about 1 year. HIV medicine can still help people at this stage of HIV infection, and it can even be lifesaving. But people who start HIV medicine soon after they get HIV experience more benefits—that’s why HIV testing is so important.

How Do I Know If I Have HIV?

The only way to know for sure if you have HIV is to get tested . Testing is relatively simple. You can ask your health care provider for an HIV test. Many medical clinics, substance abuse programs, community health centers, and hospitals offer them too. If you test positive, you can be connected to HIV care to start treatment as soon as possible. If you test negative, you have the information you need to take steps to prevent getting HIV in the future.

To find an HIV testing location near you, use the HIV Services Locator .

HIV self-testing is also an option. Self-testing allows people to take an HIV test and find out their result in their own home or other private location. With an HIV self-test, you can get your test results within 20 minutes. You can buy an HIV self-test kit at a pharmacy or online. Some health departments or community-based organizations also provide HIV self-test kits for a reduced cost or for free. You can call your local health department or use the HIV Testing and Care Services Locator to find organizations that offer HIV self-test kits near you. (Contact the organization for eligibility requirements.)

Note: State laws regarding self-testing vary and may limit availability. Check with a health care provider or health department Exit Disclaimer for additional testing options.

Learn more about HIV self-testing and which test might be right for you .

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HIV Overview

Hiv and aids: the basics.

• The human immunodeficiency virus (HIV) is the virus that causes HIV infection. If untreated, HIV may cause acquired immunodeficiency syndrome (AIDS) , the most advanced stage of HIV infection.
• People with HIV who are not on medication and do not have consistent control of their HIV can transmit HIV through vaginal or anal sex, sharing of needles, pregnancy, and/or breastfeeding. If HIV is controlled, the risk of transmission is close to zero.
• Antiretroviral therapy (ART) is the use of HIV medicines that reduce the level of HIV in the blood (called viral load). ART is recommended for everyone who has HIV. ART cannot cure HIV infection, but HIV medicines help people with HIV have about the same life expectancy as people without HIV.
• HIV medicines (ART) can eliminate the risk of HIV transmission . For parents with HIV that want to breastfeed, the risk of transmitting HIV through breast milk is less than 1% with the consistent use of HIV medicine (ART) and an undetectable viral load.
• People on ART take a combination of HIV medicines (called an HIV treatment regimen ) every day (pills) or by schedule (injections). In many cases oral medicines may be combined into a single pill or capsule. There are newer long-acting medicines given by an injection every 2 months that may be used in some people.

What is HIV and AIDS?

HIV stands for human immunodeficiency virus , which is the virus that causes HIV infection. The abbreviation “HIV” can refer to the virus or to HIV infection.

AIDS stands for acquired immunodeficiency syndrome . AIDS is the most advanced stage of HIV infection.

HIV attacks and destroys the infection-fighting CD4 cells ( CD4 T lymphocyte ) of the  immune system . The loss of CD4 cells makes it difficult for the body to fight off infections, illnesses, and certain cancers. Without treatment, HIV can gradually destroy the immune system, causing health decline and the onset of AIDS. With treatment, the immune system can recover.

How is HIV transmitted?

HIV can be transmitted from one person to another when certain bodily fluids are shared between people. Bodily fluids that can transmit HIV include blood, semen (“cum”), pre-seminal fluid (“pre-cum”), vaginal fluids, rectal fluids, and breastmilk. HIV can be transmitted during vaginal or anal sex, through sharing needles for injecting drugs or tattooing, by getting stuck with a needle that has the blood of someone with HIV on it, through pregnancy, and through breastfeeding.

The transmission of HIV from a birthing parent with HIV to their child during pregnancy, childbirth, or breastfeeding is called perinatal transmission of HIV. For more information on perinatal transmission, read the HIVinfo fact sheet on  Preventing Perinatal Transmission of HIV .

You cannot get HIV by shaking hands or hugging a person who has HIV. You also cannot get HIV from contact with objects, such as dishes, toilet seats, or doorknobs, used by a person with HIV. HIV is not spread through the air or water or by mosquitoes, ticks, or other insects. Use the HIVinfo You Can Safely Share…With Someone With HIV  infographic to spread this message.

What is the treatment for HIV?

Antiretroviral therapy (ART) is the use of HIV medicines to treat HIV infection. People on ART take a combination of HIV medicines (called an HIV treatment regimen ) every day (pills) or by schedule (injections). In many cases oral medicines may be combined into a single pill or capsule. There are newer long-acting medicines given by an injection every 2 months that may be used in some people.

ART is recommended for everyone who has HIV. ART prevents HIV from multiplying, which reduces the amount of HIV in the body (called the  viral load ). Having less HIV in the body protects the immune system and prevents HIV infection from advancing to AIDS. ART cannot cure HIV, but HIV medicines can help people with HIV live long, healthy lives.

How can a person reduce the risk of transmitting HIV?

ART reduces the risk of HIV transmission. ART can reduce a person’s viral load to an undetectable level. An  undetectable viral load  means that the level of HIV in the blood is too low to be detected by a viral load test . People with HIV who maintain an undetectable viral load have no risk of transmitting HIV to their HIV-negative partner through sex.

HIV medicines taken during pregnancy, childbirth, and breastfeeding can also reduce the risk of perinatal (parent to infant) transmission of HIV. Previously, replacement feeding (properly prepared formula or pasteurized donor human milk from a milk bank) was recommended instead of breastfeeding since the risk of HIV transmission was considered high. Now, there is evidence that the risk of transmission through the breastmilk of someone consistently using ART and maintaining an undetectable viral load is low (less than 1%). Pregnant people with HIV can speak with their health care provider to determine what method of feeding their baby is right for them.

How can a person reduce the risk of getting HIV?

For people without HIV, there are several ways to reduce the risk of acquiring (getting) HIV infection.  Using condoms correctly with every sexual encounter, particularly with partners that are HIV positive with a detectable viral load or with partners whose HIV status is unknown, can reduce the risk of acquiring HIV. Reducing HIV risk also involves limiting and reducing sexual partners, and avoiding sharing needles.

Persons who do not have HIV should talk to their health care provider about pre-exposure prophylaxis (PrEP) . PrEP is an HIV prevention option for people who do not have HIV but who are at risk of becoming infected with HIV. PrEP involves taking a specific HIV medicine every day or a long-acting injection. For more information, read the HIVinfo fact sheet on Pre-exposure Prophylaxis (PrEP) .

What are the symptoms of HIV and AIDS?

Within 2 to 4 weeks after infection with HIV, some people may have flu-like symptoms, such as fever, chills, or rash. The symptoms may last for a few days to several weeks. Other possible symptoms of HIV include night sweats, muscle aches, sore throat, fatigue, swollen lymph nodes, and mouth ulcers. Having these symptoms does not mean you have HIV. Other illnesses can cause the same symptoms. Some people may not feel sick during early HIV infection (called acute HIV ). During this earliest stage of HIV infection, the virus multiplies rapidly. After the initial stage of infection, HIV continues to multiply but at lower levels.

More severe symptoms of HIV infection for persons not on ART may not appear for many years until HIV has developed into AIDS. People with AIDS have weakened immune systems that make them prone to opportunistic infections. Opportunistic infections are infections and infection-related cancers that occur more frequently or are more severe in people with weakened immune systems than in people with healthy immune systems.

Without treatment, HIV transmission is possible at any stage of HIV infection—even if a person with HIV has no symptoms of HIV.

How is AIDS diagnosed?

Symptoms such as fever, weakness, and weight loss may be a sign that a person’s HIV has advanced to AIDS. However, a diagnosis of AIDS is based on the following criteria:

• A drop in CD4 count to less than 200 cells/mm 3 . A CD4 count measures the number of CD4 cells ( CD4 T lymphocyte ) in a sample of blood. OR
• The presence of certain opportunistic infections.

Although an AIDS diagnosis indicates severe damage to the immune system, HIV medicines can still help people at this stage of HIV infection.

This fact sheet is based on information from the following sources:

From Centers for Disease Control and Prevention:

• AIDS and Opportunistic Infections
• HIV and Perinatal Transmission

From the Department of Health and Human Services (HHS):

• Introduction
• Infant Feeding for Individuals with HIV in the United States

From the National Institute of Allergy and Infectious Diseases (NIAID):

Also see the  HIV Source  collection of HIV links and resources.

The Origins of HIV/AIDS

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• Adrian Flint  

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Why has Africa suffered so disproportionately from HIV/AIDS? This is the question at the heart of this study. One possible explanation relates to the origins of HIV, the virus that causes AIDS. The bald statistics bear repeating: by late 2008, an estimated 33.4 million people were infected with HIV/AIDS worldwide. Sufferers in sub-Saharan Africa made up two-thirds of this total (UNAIDS 2009a). That HIV originated in Africa is, conspiracy theories aside, undisputed. This being the case, it is hardly surprising that HIV/AIDS managed to gain a strong foothold on the continent. After all, HIV was not identified positively until 1983 and even then remained little understood for some years. A simple answer, therefore, to the question of ‘why Africa?’ is that Africa represents ‘ground zero’ (Iliffe 2006).

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Flint, A. (2011). The Origins of HIV/AIDS. In: HIV/AIDS in Sub-Saharan Africa. Palgrave Macmillan, London. https://doi.org/10.1057/9780230302051_3

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Research Into the Causes of HIV Essay

There is no doubt that HIV is one of the major pandemics in the world. We have investigated several main causes of this pandemic and we have come up with possible prevention measures. However, according to current health reports, the disease of HIV is still spreading at an alarming rate and the treatments are either ineffective or hard to reach by people who really need them. By conventional economical theory, the investment in education or any other encouragement to human capital/stock increase total productivity and improve general economy of a nation. However, this is not the case in Zimbabwe. It is because the HIV pandemic in this country used to be so severe that people were dying much faster than they could be trained into productive members in society. In such harsh environment, any kind of contingency plan including education and health care plan is pointless since the country cannot even support its citizens’ physiological needs according to Maslow’s hierarchy of needs. When a region is suffering from massive population loss, human’s basic survival instinct start emerging and as a result of this, people reproduce more offspring. Moreover, because the HIV is a sexually transmitted disease, the more people reproduce, the faster the disease spreads. Eventually, the situation will become a never ending loop where massive population die-out shall have become a routine. In recent years, several national governments have been working with NGOs to make a few progressive changes in Zimbabwe to cure or mitigate the current HIV pandemic.

Prevention measures for HIV in Zimbabwe and the rest of slow developing countries are given the first priority by health care professionals. Most of these prevention measures and policies are carried out by the collaborative work of governments and several NGOs and the results are very promising. Moreover, although the situation of HIV pandemic is improving in a positive way, scientists around the world are developing several experimental treatments that can effectively work in a country like Zimbabwe. Below are a few factors which can ease the financial crisis or physical/psychological problems for people are already infected with HIV:

Financial solution: land acquisition and redistribution

People need financial income and basic nutritional supply to survive. People who live in a country where they cannot support their basic needs can hardly consider treating HIV as their first priority. One of the most effective ways of solving the two problems is to provide HIV infected citizens with their own ways of achieving financial independence. The process of acquiring agricultural lands, which mostly are relic of colonial era, and redistributing them to people who are really in need them is showing promising results. This policy has been successfully implemented in some parts of Zimbabwe, and once the civilians’ lifestyles get back on track, an implementation of a more proactive practice will have high successful rate.

Medical solution: Vitamin supplement

Though HIV is still incurable in modern days, one of the problems that people in slow developing countries face is high death rate from HIV due to the lack of funds for purchasing effective medication and treatment. Thus, scientists have set up some experiments in Vietnam and realized that by giving the right dosage of vitamin supplements to the victims of HIV, their syndrome become controllable. Since vitamin supplements are cheap and widely available, this treatment method has a high potential to help thousands of people to ease the pain of their syndromes.

Solution for improving quality of life: education and psychological consultant

HIV victims are suffering from not only physiological pain but also face discriminations from both friends and families. A study done in Jamaica about sexual stigma and sympathy towards HIV victims showed that people offer their help differently towards different HIV infected people. Moreover, the report also showed that sex workers, drug addicts and homosexual people are receiving less sympathy and attention that are in fact required together with close medical attention for preventing the spread of HIV. Education is the key solution to this problem. Eliminating public stigma towards the minority requires extensive public education, introduction of social and sexual studies in schools and creating public awareness through public service announcements. In addition, medical scientists had conducted an experiment on school teenagers with a social study project called PhotoVoice in Botswana. The assignment required each student to tell a story about the pictures they took for victims of HIV. As the result, this technique has been proven effective for raising the awareness of the danger of HIV.

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• HIV is a virus that attacks the body's immune system.
• The only way to know if you have HIV is to get tested.
• There are many ways to prevent HIV, like using PrEP, PEP, condoms and never sharing needles.
• HIV treatment helps people live long, healthy lives and prevents HIV transmission.

HIV (human immunodeficiency virus) is a virus that attacks the body's immune system. Without treatment, it can lead to AIDS (acquired immunodeficiency syndrome).

There is currently no effective cure. Once people get HIV, they have it for life. But proper medical care can control the virus.

People with HIV who get on and stay on effective HIV treatment can live long, healthy lives and protect their partners.

Most people have flu-like symptoms within 2 to 4 weeks after infection. Symptoms may last for a few days or several weeks.

Having these symptoms alone doesn't mean you have HIV. Other illnesses can cause similar symptoms.

Some people have no symptoms at all. The only way to know if you have HIV is to get tested .

How it spreads

Most people who get HIV get it through anal or vaginal sex, or sharing needles, syringes, or other drug injection equipment.

Only certain body fluids can transmit HIV. These fluids include:

• semen ( cum ),
• pre-seminal fluid ( pre-cum ),
• rectal fluids,
• vaginal fluids, and
• breast milk.

These fluids must come in contact with a mucous membrane or damaged tissue or be directly injected into the bloodstream (from a needle or syringe) for transmission to occur.

Factors like a person's viral load, other sexually transmitted infections, and alcohol or drug use can increase the chances of getting or transmitting HIV.

But there are powerful tools that can help prevent HIV transmission .

Today, more tools than ever are available to prevent HIV.

Prevention strategies include:

• Using condoms the right way every time you have sex.
• Never sharing needles, syringes, or other drug injection equipment.
• Using PrEP (pre-exposure prophylaxis) and PEP (post-exposure prophylaxis).

If you have HIV, there are many ways to prevent transmitting HIV to others, including taking HIV treatment to get and keep an undetectable viral load.

The only way to know your HIV status is to get tested. Knowing your status gives you powerful information to keep you and your partner(s) healthy.

There are many options for quick, free, and painless HIV testing. If your test result is positive , you can take medicine to treat HIV to help you live a long, healthy life and protect others. If your test result is negative , you can take actions to prevent HIV .

Get tested for HIV‎

HIV treatment (antiretroviral therapy or ART) involves taking medicine as prescribed by a health care provider. You should start HIV treatment as soon as possible after diagnosis.

HIV treatment reduces the amount of HIV in the blood ( viral load ). HIV treatment can make the viral load so low that a test can't detect it ( undetectable viral load ). If you have an undetectable viral load, you will not transmit HIV to others through sex. Having an undetectable viral load also reduces the risk of HIV transmission through sharing drug injection equipment, and during pregnancy, labor, and delivery.

How it progresses

When people with HIV don't get treatment, they typically progress through three stages. But HIV treatment can slow or prevent progression of the disease. With advances in HIV treatment, progression to Stage 3 (AIDS) is less common today.

Stage 1: Acute HIV Infection

• People have a large amount of HIV in their blood and are very contagious.
• Many people have flu-like symptoms.
• If you have flu-like symptoms and think you may have been exposed to HIV, get tested .

Stage 2: Chronic HIV Infection

• This stage is also called asymptomatic HIV infection or clinical latency.
• HIV is still active and continues to reproduce in the body.
• People may not have any symptoms or get sick during this phase but can transmit HIV.
• People who take HIV treatment as prescribed may never move into Stage 3 (AIDS).
• Without HIV treatment, this stage may last a decade or longer, or may progress faster.
• At the end of this stage, the amount of HIV in the blood ( viral load ) goes up and the person may move into Stage 3 (AIDS).

Stage 3: Acquired Immunodeficiency Syndrome (AIDS)

• The most severe stage of HIV infection.
• People receive an AIDS diagnosis when their CD4 cell count drops below 200 cells per milliliter of blood, or they develop certain illnesses (sometimes called opportunistic infections).
• People with AIDS can have a high viral load and may easily transmit HIV to others.
• People with AIDS have damaged immune systems.
• They can get an increasing number of other serious illnesses.
• Without HIV treatment, people with AIDS typically survive about three years.

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Learn about HIV and how the virus is transmitted, how to protect yourself and others, and how to live well with HIV. Also learn how HIV impact the American people.

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• Published: 01 December 2021

Research priorities for an HIV cure: International AIDS Society Global Scientific Strategy 2021

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• Thumbi Ndung’u 9 , 10 , 11 ,
• Jeremy Sugarman   ORCID: orcid.org/0000-0001-7022-8332 12 ,
• Caroline T. Tiemessen   ORCID: orcid.org/0000-0002-0991-1690 13 ,
• Linos Vandekerckhove   ORCID: orcid.org/0000-0002-8600-1631 14 ,
• Sharon R. Lewin   ORCID: orcid.org/0000-0002-0330-8241 15 , 16 , 17 &

The International AIDS Society (IAS) Global Scientific Strategy working group

Nature Medicine volume  27 ,  pages 2085–2098 ( 2021 ) Cite this article

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Despite the success of antiretroviral therapy (ART) for people living with HIV, lifelong treatment is required and there is no cure. HIV can integrate in the host genome and persist for the life span of the infected cell. These latently infected cells are not recognized as foreign because they are largely transcriptionally silent, but contain replication-competent virus that drives resurgence of the infection once ART is stopped. With a combination of immune activators, neutralizing antibodies, and therapeutic vaccines, some nonhuman primate models have been cured, providing optimism for these approaches now being evaluated in human clinical trials. In vivo delivery of gene-editing tools to either target the virus, boost immunity or protect cells from infection, also holds promise for future HIV cure strategies. In this Review, we discuss advances related to HIV cure in the last 5 years, highlight remaining knowledge gaps and identify priority areas for research for the next 5 years.

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Modern antiretroviral regimens can effectively block HIV replication in people with HIV for decades, but these therapies are not curative and must be taken for life. However, there is evidence that a cure can be achieved; initially, this came from a single case study (Timothy Brown, a man living with HIV who became widely known as the ‘Berlin patient’) following bone-marrow transplantation from a donor who was naturally resistant to HIV 1 . On the basis of this inspiring development and the recognition that not everyone can access and/or adhere indefinitely to antiretroviral therapy (ART), a global consensus emerged approximately 10 years ago that a curative intervention was a high priority for people with HIV and would be necessary to bring an end to the HIV pandemic. Since then, there has been a second case report of a cure following bone-marrow transplantation 2 as well as evidence of persistence of only defective forms of the virus in certain patients 3 and enhanced immune control of the virus by others after only a short time on ART 4 —further supporting the notion that a cure for HIV can be achieved.

An HIV cure includes both remission and eradication. Here, we define the term remission as durable control of virus in the absence of any ongoing ART. Eradication is the complete removal of intact and rebound-competent virus. The minimal and optimal criteria for an acceptable target product profile for an HIV cure, including the duration and level of virus control off ART, has recently been developed and published by the International AIDS Society (IAS), following wide consultation with multiple stakeholders 5 .

In 2011 and 2016, the IAS convened expert working groups to outline a strategy for developing an effective and scalable cure 6 , 7 . Since then, significant progress has been made, and the overall agenda has evolved. Here, we assembled a group of experts from academia, industry, and the community (Box 1 ) to evaluate recent progress and to outline cure-related research priorities for the next 5 years. The key recommendations for each component of the strategy are summarized in Box 2 .

Box 1 The Global Cure Strategy—forming a consensus

The Global Cure Strategy was created using a full online process during the COVID-19 pandemic from November 2020 to August 2021. The co-chairs of the initiative identified the major topics which were divided into eight subthemes, each with its own working group, which included a chair, three scientific experts, at least one community member, an IAS Research-for-Cure fellow, and an industry representative. Working groups met at least twice virtually to generate a summary of key advances and recommendations for the next five years. The steering committee consisted of the chairs of each working group, the co-chairs of the cure strategy and a community expert, selected for diversity in geographic background, gender, age, and expertise. We engaged people living with HIV at all levels as well as a wide range of scientific and nonscientific stakeholders.

The Global Cure Strategy was further refined through a broad, online stakeholder consultation, including an online survey, a review by key stakeholders in the field, and interviews with select experts and opinion leaders (more than 25 respondents). The survey received 162 responses, primarily from people working in academia, nongovernmental organizations, and hospitals or research institutions; 11% of respondents were from organizations of people living with HIV, and 4% were from industry. The majority of respondents were working in Africa, followed by Western and Central Europe, North America, and Central and South America. The summary and detailed responses can be found here: https://www.surveymonkey.com/results/SM-7YYFTZ599/.

Box 2 Key research goals to be addressed in the next 5 years

Understanding hiv reservoirs.

Define and characterize the sources of the replication- and rebound-competent viruses during ART

Define the phenotype of cells harboring intact HIV genomes

Define the clinical significance of defective yet inducible proviruses

Define the mechanisms of clonal proliferation

Determine if infected cells that persist on ART are resistant to cell death

Define the impact of sex and other factors on the reservoir and virus-specific therapies

HIV reservoir measurement

Develop and validate a high-throughput assay to quantify the rebound-competent reservoir

Develop assays that quantify integration sites

Develop assays that account for key qualitative differences in viral transcripts

Develop methods to quantify HIV protein expression in cells and tissues

Develop imaging modalities that quantify the size, distribution, and activity of the reservoir in tissues

Define the link between the cellular reservoirs, residual plasma viremia, and the rebounding virus

Develop assays for point-of-care and eventually at-home viral-load monitoring

Mechanisms of virus control

Identify the mechanisms that contribute to SIV/HIV control

Define the role of HIV-specific antibodies, B cells, and the innate immune response in virus elimination or control

Define the viral dynamics and biomarkers associated with post-treatment control

Optimize human organoid models, as well as mouse and nonhuman primate models, for cure- and remission-related studies

Targeting the provirus

Develop improved strategies to reverse latency

Develop strategies to permanently silence the provirus

Determine the impact of targeting the provirus at the time of initiation of ART

Define the role of viral subtype on the effectiveness of interventions that target the provirus

Targeting the immune system

Develop ‘reduce and control’ approaches

Develop immune modulators

Conduct clinical trials to determine whether combination immunotherapies will result in safe and durable HIV remission

Cell and gene therapy

Define the level of antigen expression needed to enable recognition of infected cells by immunotherapies

Develop gene-editing strategies that target the provirus

Develop strategies for sustained production in vivo of antiviral antibodies

Leverage advances in other biomedical fields to develop safer and more scalable approaches

Pediatric remission and cure

Characterize the establishment, persistence, and potential for preventing or reversing HIV latency in infants and children on ART

Develop assays to monitor and identify biomarkers to predict the efficacy of HIV-1 cure therapeutics

Test HIV immunotherapies and other strategies in infants and children

Social, behavioral, and ethical aspects of cure

Expand community/stakeholder engagement and capacity building

Develop HIV cure research with equity, representation, and scalability considerations

Establish standards for the safe conduct of clinical research

Integrate social, behavioral, and ethics research as part of HIV cure trials

Build capacity for basic discovery research and clinical trials in high-burden, resource-limited settings

A shared definition of the HIV reservoir is crucial for researchers, clinicians, and people living with HIV. Here, we use the term ‘HIV reservoir’ in the context of eradication or remission, as a representative term for all cells infected with replication-competent HIV in both the blood and different anatomical sites in individuals on ART—in other words, all potential sources of viral rebound in the context of a treatment interruption. Although the source of virus rebound is still not entirely understood, we now know that virus can persist in multiple forms, in multiple cells and in multiple sites.

Characterization of the complete HIV reservoir

HIV DNA can be detected in CD4 +  T cells in blood and lymphoid tissue in nearly all people with HIV on ART. These viral genomes are mainly defective. Only a small proportion (less than 5%) appear to be intact and potentially replication-competent 8 . But the HIV reservoir goes beyond circulating CD4 +  T cells; it also includes tissue-resident CD4 +  T cells and cells of the monocyte/macrophage lineage, further complicating efforts to characterize and quantify it. In vitro, HIV preferentially integrates into transcriptionally active genes 9 ; however, in people with HIV on ART, many proviruses (defined as virus that is integrated into the host genome), including intact ones, have been identified in genomic regions that are silent (known as ‘gene deserts’), which limits or precludes their reactivation 3 .

Our initial conception of the HIV reservoir as a static viral archive has given way to a more dynamic view in which, over time on ART, certain within-host HIV variants are gradually eliminated while others persist through various mechanisms, including clonal expansion of infected cells 10 , 11 , 12 , 13 , 14 , 15 . Sporadic infection of new cells during ART has been reported 16 , although there has been no convincing demonstration that viral sequences evolve during effective ART 17 , suggesting that the degree of virus spread is minimal. The sources of viral rebound following cessation of ART are incompletely defined. Multiple factors can contribute to viral replication following ART, including anatomical and microanatomical locations, the infected cell type, cellular phenotype, the nature of the provirus, the antigen specificity of the infected cell, the potential for transcriptional activity given the specific integration site, and/or distribution of antiretroviral drugs within tissues (Fig. 1 ).

The HIV reservoir can be defined across a number of dimensions, including: (1) anatomical and microanatomical locations, (2) cell type (for example, CD4 + T cell or macrophage), (3) cell functional profile (activated or resting; resistance to killing), (4) pool of proviruses with a particular functional profile (for example, interferon-alpha resistant) or (5) triggering event (for example, response to stimulation with a particular antigen), and (6) integration-site features of the rebounding virus.

We recommend prioritizing efforts to understand integration sites of the virus during long-term ART and to understand the inducibility of a provirus on the basis of its chromosomal context. In addition, large prospective studies incorporating analytical treatment interruptions (ATIs) are still needed to probe clinically relevant sources of viral rebound and to identify a biomarker that predicts this. A favorable cure intervention could either prolong the time to the point when virus is detectable (that is, rebound) in plasma or reduce the viral ‘set point’ (that is, post-treatment control).

One of the most daunting obstacles to designing more effective methods to target persistent HIV infection is the lack of biomarkers to unambiguously identify the cells that harbor the rebound-competent reservoir. Recent work has demonstrated that the viral reservoir is preferentially enriched in cells that express programmed death-1 (PD-1) and other immune checkpoint markers, activation markers such as HLA-DR, and chemokine receptors such as CCR6 and CXCR3, but there is no phenotypic marker specific for the reservoir 18 , 19 , 20 , 21 . Specific biomarkers of the reservoir are needed, particularly to assess the impact of cure interventions. Furthermore, understanding how HIV persists in specific tissue sites and relevant local cell populations, such as those in the brain, gastrointestinal tract liver, or genital tract, will be important, given that the mechanism for persistence in each site may be distinct, and therefore different approaches may be required to eliminate each of these reservoirs.

There is growing evidence that some defective proviruses can produce transcripts and proteins (including novel viral RNAs and chimeric viral proteins) that in turn can elicit immune responses and perhaps contribute to chronic inflammation 22 , 23 , 24 , 25 . This may be of high relevance to end organ complications, such as HIV-associated neurological disease 26 . If the production of RNA and proteins from these defective proviruses proves to have clinical relevance, then their removal may be necessary to ensure long-term health.

A major mechanism of HIV persistence is the proliferation of cells that were infected prior to ART, resulting in large clonal populations of infected cells that arise as a result of the site of HIV integration 27 , 28 , response to antigen 29 , 30 , or homeostatic drivers 31 . Characterization of these presumably physiological expansions might lead to the development of therapies aimed at interrupting proliferation of infected cells. It will be important to determine to what degree these expanded clones are transcriptionally active, whether they are an important of post-ART viral rebound, and whether they have some innate survival advantage that prevents the cells from being effectively cleared by the host.

Recent studies have provided some evidence for preferential survival of infected cells with proliferative advantages or with deeper viral latency. Prosurvival and immune-resistance profiles may be particularly important in infected cells that persist despite expression of viral RNA or proteins 32 , 33 , 34 . Opportunities likely exist for collaboration and cross-fertilization of concepts with the cancer field, where the clonal dynamics of tumors have been extensively studied in relation to prosurvival and immune-resistance advantages, such as the work being done on lung cancer through prospective genetic studies in TRACRx ( https://clinicaltrials.gov/ct2/show/NCT01888601 ).

Biological sex can influence HIV pathogenesis, the immune response to HIV infection, and response to antiviral therapy 35 . Furthermore, in some but not all studies, women’s reservoirs have been shown to be less transcriptionally active and less inducible than those of men 36 , 37 , 38 , 39 , 40 . Sex, therefore, is a critical variable that should be considered as new therapies to target the reservoir are developed.

Quantification of the HIV reservoir

Significant progress toward a cure for HIV depends on having sensitive, specific, and quantitative measures of persistent virus that can be applied to various anatomical compartments 41 . Achieving this has been challenging, however, owing to the many sources and heterogeneous properties of persistent, replication-competent HIV. The reservoir can be quantified using assays that measure viral nucleic acid (total and integrated DNA, intact and defective DNA, or different forms of RNA), virus protein (p24), or viral inducibility (by measuring HIV RNA or virus replication following activation in vitro). Each approach has advantages and limitations, and assay outcomes may not always be interchangeable, comparable, or even correlated 8 .

Several groups have developed droplet digital PCR-based assays that discriminate genetically intact proviruses from a large background of defective proviruses, which are slightly less accurate but more high throughput than full genome sequencing 42 , 43 . The application of these assays to large clinical cohorts has demonstrated that there is a modest decrease in the frequency of cells with intact provirus over years on ART 44 , 45 , 46 . These assays have largely been optimized for subtype B virus, the major HIV subtype found in the United States and Europe. Yet there are over ten subtypes worldwide, some of which have evolved different mechanisms for immune evasion and persistence 47 . Pan-subtype-specific assays will need to be developed, and challenges related to cost and scalability remain. Research in this field should ideally culminate in harmonization across laboratories and crossvalidation of results. Future work will need to expand from quantification of virus in blood to quantification in tissue, particularly the more accessible tissues such as lymph nodes and gut mucosa.

Understanding the proviral landscape (defined as the degree of intactness, its transcriptional activity, and its location) is crucial, as these characteristics almost certainly influence the degree to which a provirus will rebound 48 . Over the last decade, several assays have been developed to analyze the exact location at which the virus integrates and whether the integrated virus is intact or defective. The ability to analyze single cells for integration site, viral sequence, and transcription is a major advance 48 ; however, these assays are expensive and low throughput. Technological advances are required to apply this more broadly to clinical samples, including assessment of interventions that target the reservoir.

Cell-associated viral RNA (CA-RNA) provides a measure of the total transcriptional activity of proviruses within a given sample. Several assays have recently been developed that quantify different RNA species, including total, elongated, unspliced, polyadenylated, and multi-spliced RNA, and these stand to give higher-resolution insights into the impact of therapeutic intervention 49 . An important unmet need is to develop approaches to distinguish transcripts arising from defective versus intact proviruses. Another shortcoming hampering broad use of RNA assays is the fact that they are subtype-sensitive. Overall, our ability to study the biology of transcriptionally active proviruses and the role of transcriptional activity as a potential biomarker needs to be further explored.

Since HIV protein expression is also required for recognition by HIV-specific T cells and other immune-based therapies, measuring and characterizing viral proteins in cells and tissues is an important step to understanding HIV persistence and might prove to be a critical determinant for the efficacy of therapies that target the HIV-infected cells directly (for example, chimeric antigen receptor (CAR) T cells or broadly neutralizing antibodies). Quantification of the p24 protein with ultrasensitive enzyme-linked immunosorbent assays can determine the efficacy of therapies that target the reservoir directly. Ultrasensitive p24 assays have emerged as useful tools 25 , but drawbacks include low levels of sensitivity compared with nucleic acid detection, overestimation of the replication-competent reservoir, and the requirement for specialized instrumentation 25 , 50 . Detection of viral envelope protein (the target of many therapeutic interventions for an HIV cure) also remains a challenge. Future strategies should leverage advances in single-cell techniques and new approaches to imaging tissue using super-resolution or expansion microscopy, together with multi-omics approaches.

Substantial progress in other fields of medicine has been made in using advanced imaging techniques to quantify rare diseased cells in tissues. On the basis of some preliminary success in nonhuman primate models 51 , efforts to use radiolabeled HIV-specific tracers and sensitive imaging modalities (for example, positron emission tomography, PET) have been initiated 52 . Similar efforts aimed at characterizing sites of inflammation or expression of specific surface markers that are associated with HIV persistence should also be a priority.

Several studies have attempted to identify sources of rebound virus by probing phylogenetic linkages with the proviral sequences present in various anatomical and cellular compartments. Success has been limited, however, in part owing to the challenging nature of obtaining full-length sequences from the limited number of infected cells in blood or tissue, as well as from plasma with low level viremia 53 . Strategies that can enhance enrichment of infected cells and/or depth of viral sequencing together with high-throughput low-cost single-cell analyses are likely to advance the field. As the RNA in circulating virions is a well-accepted surrogate marker for untreated HIV disease, this measurement could be an effective tool to characterize the rebound-competent population of HIV-infected cells.

Currently, any impact of a therapeutic intervention on the viral reservoir can only be determined with an ATI. A tool for very early detection of viral rebound post-ART using a nonvirological marker—such as measures of the innate immune response 54 —could be very valuable. In addition, better ways to monitor viral load that do not require frequent healthcare appointments will be needed 5 . This should include the development of home-based tests that may not necessarily require high sensitivity as long as testing is performed frequently 55 . Finally, emerging evidence suggests that virus replication during an ATI may be associated with some long-term adverse events 56 , so careful follow up of participants in ATI studies will be necessary.

Mechanisms and models of virus control

Natural control in people living with hiv.

Individuals who naturally control HIV in the absence of any therapy and can maintain a viral load of <50 copies/ml (known as ‘elite’ controllers) have been the focus of intense investigation for years. Research in this area is increasingly focused on those controllers who exhibit remarkably stringent control (‘exceptional’ controllers) 57 , 58 , some of whom might be considered true cures 48 , 59 , and those who became controllers after ART interruption (post-treatment controllers) 60 , 61 . In exceptional controllers, the frequency of infected cells is extremely low, often below the limit of detection of most standard assays for HIV DNA 57 , 59 , there is no intact virus 48 and the site of HIV integration may be distinct 48 ; an agreed definition for an exceptional controller is needed.

Virus-specific CD8 +  T cells targeting particularly vulnerable or conserved epitopes are generally recognized as the key mediator of elite control; such cells are rare in post-treatment controllers and have not yet been characterized in exceptional controllers 4 , 62 . Further characterization of the various controller phenotypes (elite, exceptional, post-treatment) should remain a priority; the identification of unique and potentially informative phenotypes should also be pursued, including individuals on ART who have very small reservoirs 62 . Functional multi-omics studies and emerging single-cell technologies should help to determine the mechanisms involved in exceptional, elite, and post-treatment control. Better animal models of exceptional and post-treatment control would greatly enhance the field, giving access to tissue and the opportunity for longitudinal assessment of virus control 63 .

Virus elimination and control will likely require a coordinated immune response involving more than just T cells. Recent data suggest that autologous antibodies targeting archived viruses as well as interferon sensitivity might influence which virus populations emerge post-ART 54 , 64 , 65 . Studies in simian immunodeficiency virus (SIV)-infected nonhuman primates that naturally control infection have provided indirect evidence that natural killer (NK) cells might be able to effectively control virus in tissues 66 . Better insights into the role of antibodies, natural killer cells, and innate immunity in post-treatment and/or post-intervention control are needed.

The interplay between the virus and immune system during acute infection or immediately after the interruption of ART is largely unknown, at least in humans. During acute infection, those destined to become controllers typically have an initial period of poorly controlled viremia 61 , 67 . For post-treatment controllers, virus control is often achieved more rapidly after cessation of ART than after primary infection 61 , 68 . We need to understand the viral dynamics associated with eventual post-ART control/remission, as this will inform how a treatment interruption should be conducted. It is likely that biomarkers other than the plasma HIV RNA level might allow for the development of safer and more cost-effective strategies for interrupting ART.

Animal models of control

The role of humanized mouse models in cure research is still evolving. Recent studies showing similar effects of latency-reversing strategies in mice and the less scalable nonhuman primate model are encouraging 69 , 70 . Given that access to nonhuman primates for cure studies will likely remain a barrier, ongoing optimization, standardization, and validation of mouse models should be prioritized.

An important discrepancy in translating cure-related findings from SIV-infected nonhuman primates to people with HIV lies in the duration of ART. Although effective ART regimens with integrase inhibitors have been optimized in nonhuman primates, high costs, and treatment-related toxicities necessitate relatively shorter study durations (less than 1–2 years of ART). One possible solution would be for primate research centers to maintain colonies of SIV-infected nonhuman primates receiving very-long-term ART to be directly assigned for studies.

There is ongoing debate about the most appropriate virus to be used in cure-related studies in nonhuman primates. Investigations utilizing broadly neutralizing antibodies or select vaccines directed against the HIV-1 envelope necessitate infection with a virus that expresses HIV envelope proteins (simian-human immunodeficiency virus, SHIV). However, SHIV infections with some strains are characterized by post-treatment control in the absence of any intervention 71 , while others can induce significant disease progression 72 . Therefore, the specific strain used can limit the generalizability of the model. Although SIV infection of nonhuman primates can cause more significant disease progression than HIV infection of people, early ART for SIV infection can limit rapid disease progression and is therefore a useful model for cure studies 73 . Developing immunotherapies that target the SIV envelope in addition to SHIV should also be pursued.

A major recent advance has been the development of genetically barcoded SIV mac239 strains 74 . Because the barcode ‘tags’ are easily quantified and also passed on to progeny virus, this model allows for tracking of clonal dynamics, providing more precise insights into how interventions affect seeding of the reservoir, viral reactivation during ART, or viral recrudescence after ART interruption.

Therapeutic interventions

Since the discovery that HIV can establish a latent infection with minimal HIV transcription, a range of approaches has emerged that specifically target latently infected cells. These include pharmacological modulation of epigenetic or signaling pathways involved in HIV transcription to reactivate latent HIV such that the cells can be targeted and eliminated (‘shock and kill’) or to permanently silence HIV transcription (‘block and lock’) 75 , 76 , 77 . Recent reports have demonstrated that HIV latency is heterogeneous and that latency reactivation is stochastic, implying that a combination of agents targeting various pathways controlling HIV transcription may be necessary to achieve either robust silencing or latency reversal 49 , 78 , 79 , 80 .

A clear limitation of the ‘shock and kill’ approach comes from the discovery that only a fraction of proviruses is intact and among these, only some are inducible by a potent stimulus such as T cell stimulation, let alone by far less potent latency-reversing agents (LRAs) 8 , 81 , 82 , 83 . Furthermore, cells containing reactivated latent HIV may also be relatively resistant to killing by cytotoxic T cells 84 . Complicating the situation even more, CD8 +  T cells appear to suppress HIV transcription and can blunt the effect of LRAs 70 .

Although LRAs tested in humans can induce HIV RNA expression and virion production in vivo, they have failed to reduce the size of the reservoir, even when combined with immunotherapeutic strategies designed to enhance clearance of infected cells 85 , 86 , 87 , 88 , 89 , 90 . This could be due to poor antigen induction by LRAs or insufficient clearance of these targets by immunotherapies (Fig. 2 ). Furthermore, many of the tested LRAs have off-target effects. Newer approaches for delivery of LRAs to reduce toxicity, enhance potency, and improve targeting, potentially leveraging advances in nanomedicine, should be explored. Greater potency could potentially be achieved using LRAs in combination, however, care is needed in these clinical trials, given that unexpected toxicities can emerge—as was recently demonstrated in the evaluation of high-dose disulfiram and vorinostat 91 . Finally, LRAs will likely need to be partnered with therapies that enhance the clearance of cells expressing viral proteins, such as immune-enhancing strategies or proapoptotic drugs 92 .

Reversing latency is an important component of revealing HIV-infected cells, allowing for conversion of a latently infected to a productively infected cell. a , Currently available LRAs reverse latency in only a subset of infected cells, and, when used alone, do not sufficiently eliminate these. b , Enhancing the efficacy of an LRA can be achieved with increased potency, targeted delivery or through using combinations of LRAs. c , Ultimately, depletion of the reservoir will require combining an LRA with other interventions, such as immunotherapy or a proapoptotic drug.

Permanently silencing the HIV promoter by suppressing factors that promote HIV transcription has also emerged as a strategy to target the provirus. The concept is to therapeutically drive HIV into a permanently silenced epigenetic state that resists reactivation (‘deep latency’). The Tat inhibitor didehydro-cortistatin A (dCA) blocks HIV reactivation from human CD4 +  T cells in vitro through epigenetic repression; treatment with dCA in ART-suppressed humanized mouse latency models induces a measurable delay in virus rebound 76 , 93 . Gene therapy can also play an important part in permanent silencing of the provirus using short interfering RNA or other modalities 94 . Thus far, these approaches have yet to be successfully translated into human trials.

Further exploration of the therapeutic potential of permanently silencing the reservoir (‘block and lock’), presumably as part of a combinatorial cure approach, is a high research priority. Some pathways that might be targeted include mTOR, HSF1, and others 95 , 96 , 97 . Efforts to screen for drugs that suppress HIV transcription are encouraged, 96 , 98 , 99 with the goal to rapidly move into preclinical and clinical studies 100 , 101 .

With a recent report indicating that the HIV reservoir is stabilized at the start of ART initiation, efforts should be devised to inhibit this stabilizing effect and/or to enhance reservoir turnover during ART, where such interventions are ideally delivered at ART initiation 102 , 103 , 104 .

Most methods to target the provirus have been developed using subtype B. Thus, while conserved mechanisms govern latency across the different virus subtypes, differences at the level of the promoter may impact responsiveness to various stimuli. Therapies targeting the provirus should be evaluated across multiple HIV subtypes including recombinants.

There is a robust and growing toolbox of immune therapies that might be advanced to proof-of-concept testing. Arguably, the most impactful innovation to date is the isolation and development of broadly neutralizing antibodies for clinical use, but advances have also been made in the development of therapeutic vaccines, vaccine adjuvants, and other immunotherapies. When used in combination in nonhuman primates, these immune therapies have resulted in sustained post-ART control 71 , 105 . When used alone, most of these approaches have had limited effectiveness in people, although some promising results are emerging 88 , 106 , 107 . Combination clinical trials have recently started and are ongoing. Although the combination of either vorinostat or romidepsin (HDAC inhibitors that can increase viral transcription through epigenetic modification) together with different HIV vaccines showed no or minimal reduction in the HIV reservoir 107 , 108 , 109 , results from other studies including a combination of Toll-like receptor agonists, LRAs and broadly neutralizing antibodies are eagerly awaited ( NCT03837756 ; NCT04319367 ; NCT03041012 ).

As it may be challenging to reactivate and eliminate all latently infected cells, or to induce deep irreversible latency in all cells, it seems unlikely that these approaches will be curative by themselves. By reducing the reservoir, however, they might make strategies aimed at controlling the virus long term post-ART more effective. This overall approach of 'reduce and control’ is supported by observations in elite and post-treatment controllers, and theoretical modeling 110 . Multiple approaches that might result in control of a small reservoir are being developed. Assessment of therapeutic vaccines including live vector vaccines such as adenovirus 26, modified vaccine Ankara, and also a cytomegalovirus in nonhuman primate models have been particularly promising, with a subset of animals achieving eradication of virus 71 , 111 . Such studies have not yet been performed in people. Research to develop and test novel immunogen and vaccine designs with broad, potent and durable immunity should be prioritized. Given the recognition that autologous neutralizing antibodies might contribute to reservoir control 64 , novel vaccine approaches aimed at the induction of broadly neutralizing antibodies—including germline targeting 112 —should also be prioritized.

Immune stimulators, immunomodulators, and novel immunotherapies (such as cytokine formulations, Toll-like receptor agonists, immune checkpoint inhibitors or agonists, and novel vaccine adjuvants), used alone or more likely in combination with other approaches, hold promise but have undergone relatively limited testing in HIV-cure studies in people so far 106 , 113 , 114 , 115 .

With the exception of a few anecdotal cases 116 , immunotherapy in people with HIV has yet to recapitulate the promising advances made in nonhuman primates. Combination of various therapies will almost certainly be needed (Fig. 3 ). Conducting such studies is feasible 108 , 117 ; it is expected that initial clinical research will be intensive in nature and designed to identify strategies that might then be tested in well-powered, controlled clinical trials. Defining the mechanisms and potential biomarkers associated with remissions/cures in the preclinical and clinical setting should remain a priority. Determining which combinations to study, and how to define the optimal doses and strategies, poses a significant challenge from a methodological and regulatory perspective. As immunotherapies for HIV move into the clinic, careful attention will have to be paid to immune-related adverse events, including cytokine-release syndrome and autoimmunity.

Strategies that will enhance immune-mediated clearance of latently infected cells include early initiation of ART and the administration of combined interventions at the time of suppressive ART (colored arrows) or during the treatment interruption phase, which will allow for increased antigen presentation. Given that there is no biomarker that can predict viral rebound, analytical treatment interruptions are used to determine whether the intervention has had a clinically meaningful impact. The overarching goal is to either delay viral rebound by at least months or years or reduce the set point of virus replication (that is, the stable level of viral load that the body settles at), preferably to a level of <200 copies/ml. The dashed colored lines represent different potential favorable outcomes from a cure intervention. bNAbs, broadly neutralizing antibodies; LRA, latency reversing agent; TLR, Toll-like receptor.

Cell and gene therapy clinical trials for people with HIV, although safe so far, have been small in scale and with no clear demonstrations of efficacy. The interest in gene therapy for an HIV cure was inspired by the elimination of intact virus in Timothy Brown (also known as the Berlin patient) and Adam Casteljo (also known as the London patient), who both received stem-cell transplants from a CCR5-negative donor 1 , 2 to treat their underlying malignancies. CCR5 is a co-receptor that is needed by most strains of HIV to enter a cell; a reduction in the size of the reservoir has also been reported following stem-cell transplantation to people with HIV from donors who are CCR5-positive 118 , 119 , but the HIV reservoir can’t be completely eliminated, irrespective of the CCR5 status of the donor. In the case of CCR5-negative stem-cell transplantation, the absence of CCR5 in the donor cells is thought to protect the newly transplanted cells from infection, at least with CCR5-dependent HIV strains. Interestingly, in both cases of cure following stem-cell transplantation of CCR5-negative cells, defective virus has been detected, but not intact or replication-competent virus 120 , 121 . These reports have prompted researchers to evaluate CCR5-targeted gene editing as a potentially safer path to cure in people living with HIV on ART, given the high mortality rate and significant morbidity associated with stem-cell transplantation. Timothy Brown unfortunately died in early 2020 owing to recurrence of his leukemia, but remained HIV-free until his death.

Ex vivo gene editing of CCR5 using zinc finger nucleases and re-infusion of CCR5-modified T cells has not yet prevented viral rebound following ATI 122 , 123 , possibly because insufficient cell numbers were engineered and/or engrafted with first-generation editing tools and cell culture protocols and/or because CCR5 disruption alone cannot shift the balance in favor of post-treatment control in the presence of persistently infected cells. More recently, gene therapies have shifted to creating effectors, including chimeric antigen receptor (CAR) T cells, which can recognize and eliminate HIV-infected cells (Fig. 4 ). Other approaches include the use of novel delivery systems to deliver genes to local tissues, resulting in the sustained production of systemically acting antivirals such as broadly neutralizing antibodies 124 , 125 and CD4 mimetics 126 . Finally, attempts are being made to directly target integrated proviruses with technologies such as CRISPR–Cas9 and recombinases 127 , 128 . This approach remains conceptually challenging in view of the disparate locations of latently infected cells, the absence of specific markers to target delivery, the heterogeneity of proviral sequences (the majority of which are defective), and the risk of off-target effects.

Examples of ex vivo (left) and in vivo (right) gene therapy approaches that have been tested in people with HIV on ART. Ex vivo strategies include gene editing to either delete or inactivate CCR5 or HIV provirus in CD4 + -enriched T cells using gene-editing tools such as zinc finger nucelases (ZFN) or CRISPR–Cas9. Alternatively, autologous T cells can be modified to express a CAR that can recognize HIV envelope, and this can then be reinfused into the participant. In vivo strategies, on the other hand, do not require external manipulation of cells; nanoparticles or viral vectors (such as adeno-associated virus (AAV)), which encapsulate mRNA or DNA, respectively, for the relevant gene to be expressed are administered directly to the patient. These approaches have recently been successful using lipid nanoparticles that contain mRNA encoding CRISPR–Cas9 135 or for expression of anti-HIV broadly neutralizing antibodies such as PG9 or VRC07 (ref. 125 ). PBMCs, peripheral blood mononuclear cells; PLWH, person living with HIV.

Many emerging cell and gene therapies are designed to target viral proteins/epitopes that are expressed in abundance on the surface of tumor cells, for example CD19 for the treatment of lymphoma 129 . Various forms of the HIV viral envelope protein (gp120 trimers and monomers, gp41) are expressed on the surface of infected cells, while multiple peptides are presented via HLA molecules. These antigens are expressed at levels well below that of many cancer antigens now being successfully targeted in the clinic. Cell-based therapies such as CAR T cells, once infused into the patient, will only persist and differentiate if there is sufficient antigenic exposure; however, the levels of antigen during ART may be too low 130 . Removal of ART after infusion of CAR T cells (or similar products) could be used to expand these cells in vivo, or more potent latency-reversing agents could be used to enhance envelope protein expression. In addition, novel adjuvants could expand CAR T cells even when the antigen burden is low, as was recently demonstrated in the nonhuman primate model 131 .

The challenges here are primarily those of delivery to relevant cells. In addition to developing methods to target specific cells, which are common problems faced by all potential in vivo gene therapies, targeting latent proviruses also presents the problem of a lack of robust cell surface markers to identify cells harboring such proviruses. Progress in both of these areas will be needed to develop strategies to deliver gene-editing reagents to latently infected cells. Some promising in vivo delivery strategies for CRISPR–Cas9 have included adeno-associated virus to target the SIV virus in nonhuman primates on ART 127 , as well as using engineered CD4 +  cell-homing messenger RNA (mRNA)-containing lipid nanoparticles in mouse models of HIV infection 132 .

Long-term in vivo secretion of antibodies or antibody-like molecules can be achieved following gene therapy vector delivery of antibody cassettes to tissues such as muscle and liver, where enhanced production of antibodies is needed, rather than specific delivery to infected CD4 +  T cells. This can be achieved through direct intramuscular injection leading to uptake in the muscle or, alternatively, intravenous injection, which will allow for uptake in the liver. Ectopic expression of these antibodies in liver or muscle cells fails to recapitulate aspects of natural antibody production, such as responsiveness to antigen and ongoing somatic hypermutation. Therefore, editing the B cell Ig locus itself to express antibodies presents an alternative and attractive gene-editing strategy 133 , 134 .

Sustained production of these antivirals could result in sustained (perhaps lifelong) control of the virus. Many barriers to success exist. Antidrug antibodies that target and clear the vectors often form rapidly 125 , limiting the ability to deliver multiple doses. Advances in mRNA encapsulation within lipid nanoparticles may potentially revolutionize delivery of gene therapy, allowing for delivery of mRNA encoding CRISPR–Cas9 and related guide RNAs in vivo, as has recently been successfully demonstrated in the treatment of transthyretin amyloidosis 135 . Also, antibodies targeting multiple antigens will likely need to be produced at high levels to prevent virus replication and escape.

Advances in T cell manufacturing are expected, driven by cancer CAR T cell therapies, which will also benefit HIV therapies. Similarly, advances occurring in gene therapy treatments for genetic diseases, such as hemoglobinopathies, are catalyzing safer and nongenotoxic conditioning for HSPC transplants, for example based on drug–antibody conjugates. Practicality will also be enhanced by moving toward using allogeneic off-the-shelf products.

Gene and cell therapies now require a shift towards a practical focus, identifying ways to expand use, reduce costs, and allow deployment in resource-limited settings. This could be achieved through abbreviated ex vivo cell manufacturing, including automated closed-system devices (‘gene therapy in a box’), to produce product in a place-of-care setting 136 . While still in the early stages of development, in vivo gene therapy also presents exciting possibilities to significantly expand access by eliminating the need for external manipulation of cells and associated technological requirements.

The unique context of perinatal HIV infection necessitates pediatric-specific strategies to achieve ART-free remission in children. The case of the Mississippi child, who started therapy ~30 hours after birth and achieved remission off ART for 27 months before virus rebounded 137 , 138 , raised the possibility that remission for children can be attained. Subsequent reports of early-treated pediatric cases with long-term (>12 years) virological control off ART have provided examples of post-treatment control in children 139 , 140 .

The nature of the reservoir in children is unique from that in adults. For example, naive CD4 +  T cells are a more important reservoir for the virus in children 141 , 142 . Further development of infant nonhuman primate models for evaluating ART and cure strategies will contribute to our understanding of the HIV reservoir and how to target it in the unique setting of infancy and immune development, but an understanding of the limitations of this model is also crucially important 141 , 142 , 143 , 144 , 145 .

Many of the recent advances in understanding HIV persistence during ART in adults, including frequency and transcriptional activity of intact virus, clonal expansion, sites of proviral integration, and inducibility, need to be applied to studies of children. Optimizing methods that can be adapted to small blood volumes are also needed.

In the context of childhood infection, clarity is needed on how latency is established in naive T cells, susceptibility of these cells to latency reversal, propensity for T cells to clonally expand, and the relative contribution of clonally expanded cells to viral rebound following cessation of ART. It is still unclear whether integration sites and reactivation potential are different in children, and whether these change with age. Given that initial studies suggest a less-inducible reservoir in cases of perinatal infection 146 , it is especially important to determine how to maximize latency reversal in children. The optimal timing of these interventions (for example, at the time of early ART initiation) could potentially limit the pool of infected cells that persist on ART; such approaches can be explored in a nonhuman primate model.

As in adults, better tools are needed to assess the impact of cure interventions in children, including quantification of HIV persistence and in-depth cellular immune profiling. There is a particular need for noninvasive tools, such as total body imaging, to assess central nervous system and other tissue-based reservoirs. It will also be important to identify biomarkers for post-treatment control, including the degree of reduction or alteration in the composition of the latent reservoir that may be predictive of pediatric remission or cure 147 . Finally, preclinical studies in infant nonhuman primates that test new interventions to reduce or eliminate persistent HIV and/or induce viral remission after ART interruption are needed to inform the development of HIV remission and cure intervention strategies. Early therapy alone is insufficient to reliably achieve a cure or long-term remission in children. Novel approaches, including earlier administration and use of more potent antiretroviral drugs, therapeutic vaccines, or other immunotherapeutics, such as broadly neutralizing antibodies and/or innate-immune-enhancing agents, will be necessary.

Research directed toward an HIV cure intertwines critical social, behavioral, and ethical aspects that must be incorporated in the scientific agenda. This research takes place within particular social contexts and communities that shape its permissibility and appropriateness. Accordingly, affected communities must be meaningfully engaged throughout the research process; social and behavioral factors must be interrogated and taken into account because they affect research feasibility, community support for the research, and the well-being of participants and other stakeholders. Research must also address the many ethical issues associated with developing a therapy, particularly since viable options for treatment are already available. Sufficient funding for research toward social, behavioral, and ethical aspects of a cure and for community involvement is therefore essential.

Substantial progress using more conceptual and normative approaches has also been made regarding the ethical issues associated with the interruption of ART 148 , 149 . Similarly, there has been attention focused on acceptable risk thresholds for research 150 . Finally, given the important role of treatment as prevention, efforts have focused on the ethics of partner-protection measures 151 .

Community engagement in HIV cure research is still suboptimal in many settings, being mostly been limited to advisory boards typically comprised of scientifically literate individuals. Capacity to discuss HIV cure research and to evaluate its potential implications for local and global communities must be built within diverse community groups. Communities should be empowered and supported through education and engagement at all levels of the research process to help shape the HIV cure research agenda and allow for potential study participants to have a voice in trial design 152 .

Since HIV cure research is highly complex and nuanced, there is also a need to ensure understanding of it among other key stakeholders, including Institutional Review Boards (IRBs) and clinicians. For example, IRBs need to appreciate the implications of ATIs for partners who they may not see as within their remit, and clinicians need to understand the rationale for ATIs in the research setting.

Attention must focus on broad representation (for example, age, race and ethnicity, gender and sexuality, geographic location, risk behaviors) in research. Diversity in participation is essential during the development of interventions aimed at complete HIV elimination or durable ART-free control. This necessitates research directed at understanding the reasons for under-representation of certain groups of people in HIV cure research. For example, cisgender and transgender women, as well as individuals of some racial and ethnic backgrounds, are less likely to participate in HIV-cure-focused clinical trials 153 . This highlights the need for more nuanced and theoretically engaged research to understand how gender, race, and other characteristics shape engagement with HIV cure research 154 . At the same time, legal and social considerations unique to each context must be identified and addressed. For example, local laws, stigma, and access to healthcare affect research involving the interruption of ART.

There is also a need to better define ethical considerations involved in the selection of populations of interest in which promising cure strategies will be tested. For example, should priority be given to testing new interventions in individuals who initiated treatment during acute infection over those who began treatment during chronic infection? What are the best means to identify and manage the ethical considerations in pediatric HIV cure research? In addition, what measures ought to be taken to ensure that recruitment is not skewed toward people with HIV in resource-limited settings? Further, ethical questions of equity and justice related to the distribution of safe and effective cure interventions must consider acceptability, scalability, and cost-effectiveness. The COVID-19 pandemic has raised unique considerations for research participants, staff, and communities 155 . Given the rapidly changing nature of the pandemic and the availability of COVID-19 vaccines and other treatments, there is a need to continually revise and assess the safety and feasibility of HIV cure research efforts.

During the study design phase, early engagement is needed in communities where research is being considered in order to determine the nature and acceptability of research-related risks. Similarly, stakeholder perceptions should be elicited to guide the development of target product profiles (the minimal and optimal characteristics of a new therapeutic intervention), as recently done for an HIV cure 5 . In especially complex clinical studies, formative research should be used to help develop a robust, informed consent process. Furthermore, nested social and behavioral research (basic, elemental, supportive, integrative) is needed to enhance understanding of the actual experiences of trial participants as well as of sexual partners of participants. These data will help provide a check on current practices, as well as provide a foundation for future efforts aimed at improving them.

Several of the key topics addressed in the previous sections are prerequisites for the development of successful cure strategies and interventions. To date, most HIV cure research has been restricted to high-income countries with relatively low HIV burden and has most often engaged men who have sex with men. HIV strains are genetically and biologically diverse, and host mechanisms of antiviral immunity required for durable control may differ by sex, geography, and ethnicity. Basic discovery research and clinical trials in resource-limited settings must be strengthened and will require enabling infrastructure development and capacity building.

In the next decade, we expect to see a greater understanding of HIV reservoirs, an increasing number of clinical trials and hopefully reports of individuals who achieved long-term remission with less intensive and more widely applicable strategies. On the basis of the current understanding and lessons from ART, it is likely that combinations of these approaches may be the first approach to be implemented. Inclusion of knowledge from fields such as oncology and COVID-19 could also greatly facilitate progress. Finally, open and responsible communication about trials and realistic expectations will remain important. Although safety is the highest priority, with increasing number of clinical trials, there is an increase in the possibility of adverse events which will need to be appropriately managed while allowing the field to advance.

This global scientific strategy, in combination with the recently developed target product profile 5 , will assist with guiding the field toward a widely applicable, acceptable, and affordable cure. The establishment of the HIV Cure Africa Acceleration Partnership 152 will hopefully enable broader engagement and facilitate rapid implementation of any successes into low- and middle-income settings. Fortunately, the resources for such work remain available, and the field is highly committed to making the long-term commitments necessary to develop an effective and scalable remission or cure strategy.

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Acknowledgements

We acknowledge the generous contribution of all the participants in the working groups, the key opinion leaders who read and provided feedback on the strategy, participants in the online survey and secretarial support from the International AIDS Society. S.R.L. and S.G.D. are funded by National Institutes of Health Delaney AIDS Research Enterprise (DARE) Collaboratory (UM1AI126611 and UM1AI164560). S.R.L. is also funded by the National Health and Medical Research Council (NHMRC; grant number GNT1149990) of Australia and the Australian Centre for HIV and Hepatitis. R.B.J. is funded by the NIH UM1AI64565. C.T.T. is funded by the South African Research Chairs Initiative of the Department of Science and Innovation and National Research Foundation of South Africa (grant 84177). O.L. is funded by the ANRS, Sidaction, University Paris Saclay, Inserm, and CEA (Commissariat à l’Energie Atomique). P.C. is funded by the NIH (HL156247 and AI164561); N.A. is funded by the NIH Delaney CARE Collaboratory 1UM1AI126619 and from R01AI134363; T.N. is funded by the South African Research Chairs Initiative of the Department of Science and Innovation and National Research Foundation of South Africa (grant 64809), The Bill and Melinda Gates Foundation (INV-033558), the International AIDS Vaccine Initiative (UKZNRSA1001) and DFG German-African Network grant (grant number AL 1043/6-1).

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University of California San Francisco, San Fransisco, CA, USA

Steven G. Deeks & Steven Deeks

UNC HIV Cure Center, Department of Medicine, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA

• Nancie Archin

University of Southern California, Los Angeles, CA, USA

• Paula Cannon

HIV i-Base, London, UK

Simon Collins

Weill Cornell Medicine, Cornell University, New York, NY, USA

• R. Brad Jones

Aidsfonds, Amsterdam, the Netherlands

Marein A. W. P. de Jong & Marein de Jong

University Paris Saclay, AP-HP, Bicêtre Hospital, UMR1184 INSERM CEA, Le Kremlin Bicêtre, Paris, France

• Olivier Lambotte

International AIDS Society, Geneva, Switzerland

Rosanne Lamplough

Africa Health Research Institute and University of KwaZulu-Natal, Durban, South Africa

• Thumbi Ndung’u

University College London, London, UK

Ragon Institute of MGH, MIT and Harvard University, Cambridge, MA, USA

Thumbi Ndung’u & Krista Dong

Berman Institute of Bioethics and Department of Medicine, Johns Hopkins University, Baltimore, MD, USA

• Jeremy Sugarman

National Institute for Communicable Diseases and Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa

• Caroline T. Tiemessen

UZ Ghent, Ghent, Belgium

• Linos Vandekerckhove

Victorian Infectious Diseases Service, The Royal Melbourne Hospital at the Peter Doherty Institute for Infection and Immunity, Melbourne, Australia

Sharon R. Lewin

Department of Infectious Diseases, Alfred Hospital and Monash University, Melbourne, Australia

Department of Infectious Diseases, The University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne, Australia

Sharon R. Lewin & Sharon Lewin

UKZN, Durban, South Africa

Zaza Ndhlovu

Centre de Recherche du CHUM and Université de Montréal, Montreal, Canada

Nicolas Chomont

BC Centre for Excellence in HIV/AIDS, Faculty of Health Sciences, Simon Fraser University, Vancouver, Canada

Zabrina Brumme

Sun Yat-sen University, Guangzhou, China

ViiV Healthcare, Branford, CT, USA

Luke Jasenosky

Treatment Action Group, New York, NY, USA

Richard Jefferys

Institut Pasteur, Université de Paris, Unité HIV, Inflammation et Persistance, Paris, France

Aurelio Orta-Resendiz

National Cancer Institute, Center for Cancer Research, Bethesda, MD, USA

Frank Mardarelli

UMC Utrecht, Utrecht, the Netherlands

Monique Nijhuis

Perelmann School of Medicine, University of Pennsylvania, Philadelphia, PA, USA

Katharine Bar & Pablo Tebas

Merck & Co., Inc., Department of Infectious Disease & Vaccines, Kenilworth, NJ, USA

Bonnie Howell

European AIDS treatment group (EATG), Zurich, Switzerland

Alex Schneider

1CONICET – Universidad de Buenos Aires. Instituto de Investigaciones, Biomédicas en Retrovirus y SIDA (INBIRS), Buenos Aires, Argentina

Gabriela Turk

Facultad de Medicina, Departamento de Microbiología, Parasitología e Inmunología, Buenos Aires, Argentina

Makerere University, Makerere, Uganda

Rose Nabatanzi

John Hopkins School of Medicine, Baltimore, MD, USA

Joel Blankson

ICATS, UNC School of Medicine, Chapel Hill, NC, USA

J. Victor Garcia

Emory University School of Medicine, Yerkes National Primate Research Center, Atlanta, GA, USA

Mirko Paiardini

ViiV Healthcare, London, UK

Jan van Lunzen

Chelsea and Westminster Hospital NHS Foundation Trust, London, UK

Christina Antoniadi

Laboratório de AIDS e Imunologia Molecular, Instituto Oswaldo Cruz, Rio de Janeiro, Brazil

Fernanda Heloise Côrtes

Scripps Research Institute, Jupiter, FL, USA

Susana Valente

Aarhus University Hospital, Aarhus, Denmark

Ole S. Søgaard

Universidade Federal de Sao Paulo, Sao Paulo, Brazil

Ricardo Sobhie Diaz

Gladstone Institute of Virology, University of California San Francisco, San Francisco, CA, USA

Melannie Ott

USAHIV Drug Discovery, ViiV Healthcare, Qura Therapeutics, and UNC HIV Cure Center, University of North Carolina at Chapel Hill, Research Triangle Park, NC, USA

Richard (Rick) Dunham

EATG, Berlin, Germany

Siegfried Schwarze

Queen’s University, Kingston, Ontario, Canada

Santiago Perez Patrigeon

MUJHU Care limited, Kampala, Uganda

Josephine Nabukenya

The Rockefeller University, New York, NY, USA

Marina Caskey

IrsiCaixa AIDS Research Institute, HUGTIP, Badalona, Barcelona, Spain

Beatriz Mothe

Chinese Academy of Sciences, National Clinical Research Center for Infectious Diseases, Division of Treatment and Care, National Center for AIDS/STD Control and Prevention, Beijing, China

Fu Sheng Wang

Imperial College London, Department of Infectious Disease, Faculty of Medicine, London, UK

Sarah Fidler

Gilead Sciences, Foster City, CA, USA

Devi SenGupta

European AIDS Treatment Group (EATG), Brussels, Belgium

Stephan Dressler

University of North Carolina Project Malawi, Lilongwe, Malawi

Mitch Matoga

Fred Hutchinson Cancer Research Center, Seattle, WA, USA

Hans-Peter Kiem

Joint Clinical Research Centre, Kampala, Uganda

Cissy Kityo

Caring Cross, Gaithersburg, MD, USA

Boro Dropulic

University of Washington, Seattle, WA, USA

Michael Louella

Advanced Medical and Dental Institute, Universiti Sains Malaysia, Pulau Pinang, Malaysia

Kumitaa Theva Das

Johns Hopkins University School of Medicine, Baltimore, MD, USA

Deborah Persaud

Emory University School of Medicine and Children’s Healthcare of Atlanta, Atlanta, GA, USA

Ann Chahroudi

University of Massachusetts, Worcester, MA, USA

Katherine Luzuriaga

Chulalongkorn University, Bangkok, Thailand

Thanyawee Puthanakit

ImmunityBio, Inc, Culver City, CA, USA

Jeffrey Safrit

Botswana Harvard AIDS Institute Partnership, Gaborone, Botswana

Gaerolwe Masheto

UNC Gillings School of Global Public Health, Chapel Hill, NC, USA

Karine Dubé

La Trobe University, Melbourne, Australia

Jennifer Power

AVAC, New York, NY, USA

Jessica Salzwedel

VARG, Chiang Mai, Thailand

Udom Likhitwonnawut

UCSD AntiViral Research Center, Delaney AIDS Research Enterprise/UCSF, Palm Springs, CA, USA

Jeff Taylor

Social Policy, Gender Identity, and Sexual Orientation Studies Association (SPoD), University of Lucerne MSc Health Sciences, Istanbul, Turkey

Oguzhan Latif Nuh

Rakai Health Sciences Program, Rakai, Uganda

Edward Nelson Kankaka

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Core Leadership Group

• Steven Deeks
• , Sharon Lewin
• , Marein de Jong
• , Rosanne Lamplough
•  & Simon Collins

Working Group 1 (Understanding HIV reservoirs)

• , Zaza Ndhlovu
• , Nicolas Chomont
• , Zabrina Brumme
• , Luke Jasenosky
• , Richard Jefferys
•  & Aurelio Orta-Resendiz

Working Group 2 (HIV reservoir measurement)

• , Frank Mardarelli
• , Monique Nijhuis
• , Katharine Bar
• , Bonnie Howell
• , Alex Schneider
• , Gabriela Turk
•  & Rose Nabatanzi

Working Group 3 (Mechanisms of virus control)

• , Joel Blankson
• , J. Victor Garcia
• , Mirko Paiardini
• , Jan van Lunzen
• , Christina Antoniadi
•  & Fernanda Heloise Côrtes

Working Group 4 (Targeting the provirus)

• , Susana Valente
• , Ole S. Søgaard
• , Ricardo Sobhie Diaz
• , Melannie Ott
• , Richard (Rick) Dunham
• , Siegfried Schwarze
• , Santiago Perez Patrigeon
•  & Josephine Nabukenya

Working Group 5 (Targeting the immune system)

• , Marina Caskey
• , Beatriz Mothe
• , Fu Sheng Wang
• , Sarah Fidler
• , Devi SenGupta
• , Stephan Dressler
•  & Mitch Matoga

Working Group 6 (Cell and gene therapy)

• , Hans-Peter Kiem
• , Pablo Tebas
• , Cissy Kityo
• , Boro Dropulic
• , Michael Louella
•  & Kumitaa Theva Das

Working Group 7 (Paediatric remission and cure)

• , Deborah Persaud
• , Ann Chahroudi
• , Katherine Luzuriaga
• , Thanyawee Puthanakit
• , Jeffrey Safrit
•  & Gaerolwe Masheto

Working Group 8: (Social, behavioral and ethical aspects of cure)

• , Karine Dubé
• , Jennifer Power
• , Jessica Salzwedel
• , Udom Likhitwonnawut
• , Jeff Taylor
• , Oguzhan Latif Nuh
• , Krista Dong
•  & Edward Nelson Kankaka

Contributions

S.G.D., S.R.L., M.D.J. and R.L. developed the method for generating the strategy and oversaw the governance and establishment of the working groups. All authors on the masthead were members of the steering group. All authors of the IAS Global Scientific Strategy writing group contributed to the writing and approved the submitted version of the manuscript. Members of the IAS Global Scientific Strategy working groups are identified in the list at the end of the manuscript.

Corresponding authors

Correspondence to Steven G. Deeks or Sharon R. Lewin .

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Competing interests.

S.G.D. receives research support from Gilead and Merck. He is a member of the scientific advisory boards for BryoLogyx, Enochian Biosciences and Tendel. He has consulted for AbbVie, Biotron, Eli Lilly, GSK/ViiV and Immunocore; J.S. is a member of Merck KGaA’s Ethics Advisory Panel and Stem Cell Research Oversight Committee; a member of IQVIA’s Ethics Advisory Panel; a member of Aspen Neurosciences Clinical Advisory Panel; a member of a Merck Data Monitoring Committee; a consultant to Biogen; and a consultant to Portola Pharmaceuticals Inc. None of these activities are related to the issues discussed in this manuscript; T.N. has received research funding from Gilead Sciences; O.L. has been paid expert testimony and consultancy fees from BMS France, MSD, Astra Zeneca; consultancy fees from Incyte, Sobi, grants from ViiV and Gilead; L.V. receives research grants from J&J, ViiV Healthcare and Gilead Sciences; P.C. is a member of Gilead’s HIV Cure Advisory Board; S.R.L.’s institution receives funding for investigator initiated research from Gilead, Merck and Viiv. She has research collaborations with BMS, Abbvie and Merck. She has received honoraria paid to her for membership of advisory boards to Gilead, Merck, Viiv, Immunocore, Vaxxinity, Biotron, Esfam and Abivax; R.L. is an employee of the International AIDS Society; M.d.J. was paid as a consultant by the International AIDS Society. S.C., R.B.J., C.T. and N.A. have no interests to declare.

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Peer review information Nature Medicine thanks Ravindra Gupta and the other, anonymous, reviewers for their contribution to the peer review of this work. Karen O’Leary was the primary editor on this article and managed its editorial process and peer review in collaboration with the rest of the editorial team.

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Deeks, S.G., Archin, N., Cannon, P. et al. Research priorities for an HIV cure: International AIDS Society Global Scientific Strategy 2021. Nat Med 27 , 2085–2098 (2021). https://doi.org/10.1038/s41591-021-01590-5

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DOI : https://doi.org/10.1038/s41591-021-01590-5

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Essay on AIDS for Students and Children

500+ words essay on aids.

Acquired Immune Deficiency Syndrome or better known as AIDS is a life-threatening disease. It is one of the most dreaded diseases of the 20 th century. AIDS is caused by HIV or Human Immunodeficiency Virus, which attacks the immune system of the human body. It has, so far, ended more than twenty-nine million lives all over the world. Since its discovery, AIDS has spread around the world like a wildfire. It is due to the continuous efforts of the Government and non-government organizations; AIDS awareness has been spread to the masses.

AIDS – Causes and Spread

The cause of AIDS is primarily HIV or the Human Immunodeficiency Virus. This virus replicates itself into the human body by inserting a copy of its DNA into the human host cells. Due to such property and capability of the virus, it is also known as a retrovirus. The host cells in which the HIV resides are the WBCs (White Blood Cells) that are the part of the Human Immune system.

HIV destroys the WBCs and weakens the human immune system. The weakening of the immune system affects an individual’s ability to fight diseases in time. For example, a cut or a wound takes much more time to heal or the blood to clot. In some cases, the wound never heals.

HIV majorly transmits in one of the three ways – Blood, Pre-natal and Sexual transmission. Transfusion of HIV through blood has been very common during the initial time of its spread. But nowadays all the developed and developing countries have stringent measures to check the blood for infection before transfusing. Usage of shared needles also transmits HIV from an infected person to a healthy individual.

As part of sexual transmission, HIV transfers through body fluids while performing sexual activity. HIV can easily be spread from an infected person to a healthy person if they perform unprotective sexual intercourse through oral, genital or rectal parts.

Pre-natal transmission implies that an HIV infected mother can easily pass the virus to her child during pregnancy, breastfeeding or even during delivery of the baby.

AIDS – Symptoms

Since HIV attacks and infects the WBCs of the human body, it lowers the overall immune system of the human body and resulting in the infected individual, vulnerable to any other disease or minor infection. The incubation period for AIDS is much longer as compared to other diseases. It takes around 0-12 years for the symptoms to appear promptly.

Few of the common symptoms of AIDS include fever , fatigue, loss of weight, dysentery, swollen nodes, yeast infection, and herpes zoster. Due to weakened immunity, the infectious person falls prey to some of the uncommon infections namely persistent fever, night sweating, skin rashes, lesions in mouth and more.

Get the huge list of more than 500 Essay Topics and Ideas

AIDS – Treatment, and Prevention

Till date, no treatment or cure is available for curing AIDS, and as a result, it is a life-threatening disease. As a practice by medical practitioners, the best way to curb its spread is antiretroviral therapy or ART. It is a drug therapy which prevents HIV from replicating and hence slows down its progress. It is always advisable to start the treatment at the earliest to minimize the damage to the immune system. But again, it is just a measure and doesn’t guarantee the cure of AIDS.

AIDS prevention lies in the process of curbing its spread. One should regularly and routinely get tested for HIV. It is important for an individual to know his/her own and partner’s HIV status, before performing any sexual intercourse activity. One should always practice safe sex. Use of condoms by males during sexual intercourse is a must and also one should restrict oneself on the number of partners he/she is having sex with.

One should not addict himself/herself to banned substances and drugs. One should keep away from the non-sterilized needles or razors.  Multiple awareness drives by the UN, local government bodies and various nonprofit organizations have reduced the risk of spread by making the people aware of the AIDS – spread and prevention.

Life for an individual becomes hell after being tested positive for AIDS. It is not only the disease but also the social stigma and discrimination, felling of being not loved and being hated acts as a slow poison. We need to instill the belief among them, through our love and care, that the HIV positive patients can still lead a long and healthy life.

Though AIDS is a disease, which cannot be cured or eradicated from society, the only solution to AIDS lies in its prevention and awareness. We must have our regular and periodical health checkup so that we don’t fall prey to such deadly diseases. We must also encourage and educate others to do the same. With the widespread awareness about the disease, much fewer adults and children are dying of AIDS. The only way to fight the AIDS disease is through creating awareness.

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• Essay on AIDS

HIV (human immunodeficiency virus) is an infection that causes cells in the body that help it fight infections, making a person more susceptible to other infections and diseases. Interaction with certain bodily secretions of an HIV-positive individual, most commonly during unprotected intercourse (sex without the use of a condom or HIV treatment to prevent or treat HIV), or sharing injection drug equipment spreads the virus.

If HIV is not treated, it can progress to AIDS (acquired immunodeficiency syndrome). HIV cannot be eradicated by the human body, and there is no effective HIV cure. As a result, whether you have HIV, you will have it for the rest of your life.

Long and Short AIDS Essay in English

There are many diseases causing microorganisms, like bacteria, viruses, fungi etc. The symptoms of the diseases depend on the type of microorganism that is spreading it. It can vary from mild to severe. AIDS which stands for Acquired Immunodeficiency Syndrome is a viral disease that is rampant in growth. It was only in the last century that this viral disease has proved to be lethal and fatal, taking away about twenty million lives globally. The awareness about the disease and the virus causing it which is HIV or Human Immunodeficiency Virus is more now compared to earlier. In this HIV AIDS essay, we can go through the important information about it and burst some myths.

Below are different ways to write an AIDS essay in English. The essay on HIV AIDS can be of 2 formats, a long essay on HIV AIDS or a short AIDS essay.

Short Essay on Aids

This AIDS essay is a brief one and will cover the important notes about the disease and the ways one can prevent it.

The way of occurrence of this disease is in the name itself, AIDS stands for Acquired Immunodeficiency Syndrome. The disease is acquired via the virus which is called Human Immunodeficiency Virus. It is not an auto-immune disease in the early stages of infection where the immune system in the body fights off infection to protect the body from diseases that go against itself. The virus enters from an outside source and destroys the efficiency of our immune system.

AIDS is transmitted through contact. The contact with infected blood of the HIV OR AIDS patient in any form can easily transfer this viral disease. It can also be transmitted through contact with semen or vaginal fluids of the infected person. This occurs in the case when one is sexually exposed to a person with HIV.

HIV once enters the body, invades and conquers the immune system making the body susceptible to other diseases. It is then very easy for the simple flu or cold infection to be severe as the immune system is no longer fit to fight it.

When detected in the early period can be battled with, but more often than not people assume the symptoms to not be AIDS so it spreads and kills the individual. To be protected when having sex and not sharing any form of toiletries with others is the way to prevent and keep this deadly virus at bay.

Long Essay on AIDS

This is the long format of an essay on HIV AIDS where its workings, causes and effects and remedies are discussed.

There are some diseases that have been borne by the living in this world which has created a ruckus in human history and the struggle to find a permanent cure still exists. AIDS is one such disease. Acquired Immunodeficiency Syndrome is the name of the disease which is also shortened as AIDS.

It has since only the 20 th century affected the human race and many people lost their lives, more than 20 million of them. The virus that aids in the transmission of this disease is Human Immunodeficiency Virus or also called HIV. Due to the same property of immunodeficiency, it is referred to as HIV/AIDS.

Since it affects the immune system severely, the cells and the workings of it in our body must be clearly understood. The immune system’s role in the body is that of a soldier wherein it identifies any sort of anomalies that enters or infiltrates the body and prepares antibodies against it. And kills them in order to prevent infection that has the probability of causing a harmful disease.

Since the cells of the immune system have already created the antibodies, the cell memory is activated when the entry occurs again and the immune system fights and destroys such foreign and harmful matter.

What Happens when HIV Enters the Body?

When a person is infected with the Human immunodeficiency virus, it directly attacks the immune system making the cells weak and incapable of creating antibodies for this particular virus. As they become weak their function to perform the task of defending against other microorganism entrants is also weakened.

When the fighter in our bodies becomes weak, we are more likely to fall ill. The illness can be a simple flu or an allergy and our body cannot fight any further. The symptoms once infected will start to appear within the first two weeks. The symptoms are very flu-like for instance, one will be more tired than usual and fatigue will be more frequent and regular. Other symptoms include sore throat and fever. The risk of opportunistic infections like tuberculosis and herpes also increases. Some people however remain asymptomatic even for longer periods after being infected with the virus.

Cause of HIV/AIDS

The main and only cause of this dreadful disease is the contact through blood, semen, pre-seminal fluid, vaginal fluids, rectal fluids and breast milk. The semen and vaginal fluids are transferred through sex and rectal fluids through anal sex. When people have multiple partners, and they have unprotected sex the transmission is highly likely. The contact through blood can also be via the unhygienic practice of sharing an infected person’s razors, blades. Even unsterilized syringes while taking drugs or even a tattoo parlor where they use unsterilized machines on the body can transmit the virus easily. The transmission means are endless so one must proceed with utmost caution to keep themselves safe either way.

What is the Life Expectancy for the Patients Carrying HIV or AIDs with Them?

Many factors can affect the life expectancy of people living with HIV. Depending on these factors there are many differences in the outcomes between people, and other factors. The factors on which life expectancy depend are:

Access to effective HIV treatment and quality health care.

Start HIV treatment as soon as possible after HIV infection, before your CD4 cell count drops to a low level. The sooner you are diagnosed and start HIV treatment, the better your long-term chances are.

Having serious HIV-related illnesses in the past. This may occur before HIV is diagnosed and/or before HIV treatment is started. These diseases have a detrimental effect on life expectancy.

Results one year after starting HIV treatment. Studies show that life expectancy is better for people who respond well within a year of starting treatment than people who do not respond. In particular, people with a CD4 count of at least 350 and an undetectable viral load during the year have a much better chance long-term.

Year of Diagnosis - HIV treatment and medical care have improved over the years. People who have been diagnosed in recent years are expected to live longer than people who were diagnosed long ago.

Heart diseases, liver diseases, cancer and other health conditions are more likely to be the cause of death than HIV or AIDs.

Injecting drug use - Life expectancy is short for people with HIV who inject drugs, due to drug overdose and viral infections.

Social and Economic Conditions - there are significant differences in life expectancy depending on where you grew up, your income, education, social status and more.

Gender – Men are supposed to live for a shorter period of time than women.

Genetics - you may have certain conditions if close relatives have.

Mental and Emotional Well-being - high levels of stress are associated with reduced life expectancy.

Lifestyle - longevity for people who eat a balanced diet, are physically active, maintain a healthy weight, avoid alcohol abuse or use drugs, and stay in touch with the community. Avoiding smoking is very important in life.

There are a few myths surrounding this disease. It is believed earlier that AIDS can spread even through contact or touch without any exchange of fluids. Like through a hug or just by being near the infected person. That myth has been debunked and it is absolutely untrue. One can freely hug an AIDS patient without worry.

The other one was when kissing, there is an exchange of saliva which is also a fluid and AIDS can spread through kissing, which also proved to be untrue. And HIV always means AIDS that is fatal was another rumor or myth, and this myth is proven wrong where many people have lived longer with HIV by medication and taking care of their health.

There is no permanent cure yet for treating HIV/AIDS, so it is our responsibility to look out for ourselves. The way one can first prevent themselves from being infected is by getting vaccinated. It is important to get tested in your adult life if you have multiple sexual partners and also get your partner tested for the same. The other way is being monogamous. The most used form of prevention is having protected and safe sex and using condoms that creates a barrier for transmission. Do check for sterilized needles in case you decide to get a tattoo or injected.  Lessen the use of alcohol and drugs as that is anyway weakening and altering the immune system.

According to the estimates of the Indian government  2.40 million Indians are living with HIV wherein, the infected ones fall in the age group of 15-49, and 39 %of them that is 9,30,00 of them are women. The numbers are alarming and the rate of increase is not slowing down anytime soon. We as a country must break the traditions and conversations about sex should be open and safe. It is high time we lose our lives to this disease which can be prevented.

FAQs on Essay on AIDS

1. Is AIDS an Autoimmune Disease?

In the early stages of HIV infection that leads to AIDS, the immune system only weakens so it is not an auto-immune disease. But during the later and final stages, the workings of the immune system are similar to that of an auto-immune system where it works against itself. And in such cases, the body of the individual is susceptible to many more diseases. AIDS, a disease found in immune deficiency disorder, is caused by HIV and weakens the human immune system. Autoimmune diseases, on the other hand, are where the immune system turns, attacking healthy cells.

2. Does one die from HIV Infection?

The HIV infection results in many symptoms that make the body weaker day by day. But some do not even suffer those symptoms and they may live longer than the ones showing severe symptoms. In any case, it is important to take medications that are prescribed to reduce the severity of symptoms and live a little longer. The best way is to keep healthy and lead an active lifestyle as much as possible. Although the death toll from AIDS has dropped dramatically around the world, this situation increases the risk of contracting a fatal disease — potentially leading to death. No treatment or cure is present for HIV.

3. What method was adopted by the hospitals to report HIV or AIDs cases?

The doctors took the active initiative for the reporting and diagnosis of HIV or AIDs cases all over the world. The methods that all the French hospital wards were known for, for their role in controlling HIV infection, were asked to report the 2000 deaths among HIV-positive adults. The causes of death were recorded using a standard questionnaire. The Mortality 2000 study was launched to explain the distribution of the leading causes of death of HIV-positive people at the national level in France in the year 2000.

4. What is the way of determining the root cause of death in AIDs patients?

Following the International Classification of Diseases, 10th Revision (ICD-10) to death, the information contained in the questionnaire was used to determine the single cause of death. The causes of AIDS were categorized as one cause of death, followed by definitions of AIDS-related diseases. If a standard questionnaire was lost, summarized quarter notices were used to determine the underlying cause of death, if possible. Determination of the AIDs cases was set to the most important things in the list, which was done from the abstracted quarterly notifications from the questionnaires.

5. Is Vedantu a reliable website for knowing about AIDs disease?

Vedantu is the most reliable website for referring to information about AIDs disease. Being one of the most dangerous diseases in the world with no proper treatment or cure, the world's physicians are still under pressure to decipher the way to save a person from this disease. The Vedantu website contains authentic or updated information about this disease and thus the readers and viewers can rely on this source of information for perfect knowledge about the disease and its prevention also.

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The social stigma of HIV–AIDS: society’s role

Emmanuel n kontomanolis.

Department of Obstetrics and Gynecology, Democritus University of Thrace, Alexandroupolis, Greece

Spyridon Michalopoulos

Grigorios gkasdaris, zacharias fasoulakis.

AIDS is a devastating and deadly disease that affects people worldwide and, like all infections, it comes without warning. Specifically, childbearing women with AIDS face constant psychological difficulties during their gestation period, even though the pregnancy itself may be normal and healthy. These women have to deal with the uncertainties and the stress that usually accompany a pregnancy, and they have to live with the reality of having a life-threatening disease; in addition to that, they also have to deal with discriminating and stigmatizing behaviors from their environment. It is well known that a balanced mental state is a major determining factor to having a normal pregnancy and constitutes the starting point for having a good quality of life. Even though the progress in both technology and medicine is rapid, infected pregnant women seem to be missing this basic requirement. Communities seem unprepared and uneducated to smoothly integrate these people in their societies, letting the ignorance marginalize and isolate these patients. For all the aforementioned reasons, it is imperative that society and medical professionals respond and provide all the necessary support and advice to HIV-positive child bearers, in an attempt to allay their fears and relieve their distress. The purpose of this paper is to summarize the difficulties patients with HIV infection have to deal with, in order to survive and merge into society, identify the main reasons for the low public awareness, discuss the current situation, and provide potential solutions to reducing the stigma among HIV patients.

Introduction

Traditionally, women have occupied positions in the health care professions. At the same time, they have also been recipients of health care services. In recent years, studies of women have greatly increased, and the subject of women and health has received a great deal of attention. Many research programs have been carried out by physicians, psychologists, sociologists, and historians. One of the topics that has been extensively studied during gestation is HIV-AIDS. AIDS is considered to be one of the most devastating infections during gestation, having both medical and ethical implications; as a result, women are trapped between social obstacles. 1 – 3

It is indisputable that mental health is the primary requirement for a healthy gestation, and the main impetus of women’s well-being. Unfortunately, women living with HIV-AIDS are quite often stigmatized; a stigma that persists to this day. This process fills them with feelings of shame and guilt, feelings that definitely do not help them maintain a good self-esteem and a healthy mental state. Women possess and guard the right to childbearing. However, HIV-positive pregnant women face depressing and suicidal thoughts, as HIV-related stigma and discrimination govern their lives. 4 The presence of stigma and discrimination inevitably leads to significant physical, psychological, and economical side effects. The stigma permeates and disintegrates social structure. 5 , 6

Numerous social issues arise considering the role of society on eliminating HIV-AIDS since the appearance of the syndrome has revealed an undercurrent of hostility and rage ( Figure 1 ). This article focuses mainly on the potential and catalytic role of stigma, the darkest facet of AIDS, and examines the major effects on childbearing subjects and the role society must play in order to eliminate HIV discrimination.

Schematic representation of the interactions among main social issues.

Society’s role and the effects of stigma

Sexuality has long been a taboo subject, but it has undergone sweeping changes over centuries. On top of that, the emergence of HIV-AIDS has overwhelmed the entire world. The specific issue of AIDS is definitely a problem that has no short-term solution. 7 – 9

Since the beginning of human existence, people have created the feeling of teamwork, formed tribes and communities, moved from place to place together, and lived in structured societies with rules of mutual respect. Illiterate people lacking the ability to navigate, lacking the wheel, or knowledge of the stars, and living a simple existence ended up creating enormous civilizations with incredible technological innovations. Despite this, technological innovations, illiteracy, racial discrimination, and economic exploitation have resulted in a major and unjustified worldwide crisis. Uneducated people can neither vote in elections nor satisfy their basic needs.

The role of women

Throughout the centuries, women have been mistreated and socially disadvantaged, living in the shadows, especially in Third World countries. The reason for this isolation is derived from sex-based distinction of difference in physique, established since antiquity. 6 The HIV infection, in addition to all the insecurity, anxiety, and fear of discrimination derived from sex-based distinction, has led people – especially women – to avoid disclosing their HIV status to anyone but their family, a globally observed phenomenon. HIV infection is associated with minorities, marginalized, racially, ethnically, or sexually differentiated groups of people. Very frequently, once women are infected, they may be rejected even by their own families. The isolation, living a life entirely different from the rest of the people, creates a remarkable degree of tension. Protection of human rights is a vital prerequisite for eliminating all types of discrimination enforced on the HIV carriers and their families and friends. These facts make information and education regarding HIV infection imperative, so that the existing stereotypes and misconceptions can be corrected. 10 – 12

Accessibility to therapy

Although there is no legal requirement for a doctor to treat any patient, fear of infection is not an ethically correct excuse for a doctor to deny therapy to an HIV-positive patient. Actions such as refusing to provide medical support and treatment to childbearing women are a major insult to human dignity. 13 , 14 But it is not only the therapists who are responsible for the lack of health provision in pregnant women; it is commonly known that a pregnant woman at high risk, even for HIV infection, is not obliged to be tested or treated against her will, even if the fetus could be adversely affected by such a decision. Therefore, it is extremely important for patients to understand the necessity of seeking help, since there is a strong correlation between physical and psychological illness. Statistics show that morbidity and mortality rates are much higher in patients who require psychiatric attention. 15 – 17

In AIDS-related medical and social situations, the right to free oneself from discrimination has received great attention. Stigma is a multifaceted social structure that has its own pathway; it starts with labeling, separation, status loss, and ends up in discrimination. It is known that the impact of vulnerability and sensitivity to stigma differ from person to person. The main goal of modern medicine is to eliminate stigmatization and discrimination and to ensure confidentiality in testing and counselling. 18 – 20

Transmission and discrimination in modern societies

In Western societies, where an excellent physical appearance combined with a perfect physique is considered ideal, the opposite is regarded as antisocial and off-putting. Societies have been changeable over time, marginalizing the mentally ill, stigmatizing them to a great extent. 21 A chronically ill or permanently impaired person is likely to be rejected by others, experiencing feelings of guilt and responsibility for being sick. In such a setting, women regarded as HIV patients are typically held responsible for their condition and, therefore, the stigma is almost inevitable, threatening their social expectations, ambitions, and progress; women have nothing to expect but barbarity. 22 For this reason, childbearing women who are experiencing long-term stigmatizing problems have to form their own strategies to deal with societal denigration and mistreatment. 23 – 25

It is a fact that the HIV virus is primarily contracted through sexual contact, breast-feeding, pregnancy, and exposure to any type of infected medical equipment. 26 It is frequently transmitted through actions that are kept secret, hidden, or are illegal – a characteristic that makes this disease unique. Misconceptions have shaped beliefs; unfortunately, most people in our society do not realize that it is not the patient’s intention to be infected by HIV. Consequently, despair, exhaustion, and helplessness approaching panic are experienced by most female patients, who are faced with society’s rejection, losing their hopes for a prosperous future. 27 , 28 It is almost impossible to conceptualize the degree of suffering the human body undergoes and the despair of the human mind in a societal group devastated by AIDS. Infected individuals are considered to be incapable of functioning normally, and in severe cases, they are forced to withdraw from occupational responsibilities. To a significant extent, they are perceived as threats, they face long-term, damaging degradation of their life style and, additionally, they have to cope with the everlasting stigma. 27 – 30

Being stigmatized and restriction of opportunities on different levels invariably accompanies chronic diseases, resulting in a period of prolonged erosion of vocations and beliefs. Societies have constantly struggled to define discrimination and achievement. Nowadays, social stigma could have been eliminated with the use of modern technology but something like that is far away from reality. Since stigma exists and people are marginalized, subjects afflicted with AIDS are expected to struggle harder to achieve in society, facing great difficulties while reaching occupational independence and success. More specifically, HIV-positive women are neglected, less socially noticeable, meaning that their rehabilitation and long-term future are given less consideration. These women are offered limited opportunities, no aspirations, and worst of all, have no prospects regarding their general societal status. Uncertainty becomes a big part of their life. 31 – 33

Living with HIV: social support and quality of life (QoL) in HIV-positive women

From the time of conception, the human organism maintains its integrity and stability through a range of cells and tissues, in a delicate cooperation with a complex network of regulatory mechanisms. Humans have adapted to difficult situations, encountered and eliminate dangerous diseases through time, many with the use of advanced knowledge and technology. 34

According to WHO, 17.4 million women were living with HIV worldwide in 2014 constituting 51% of all adults living with HIV. 35 Fortunately, from 2001 to 2013, the annual number of new HIV infections has declined by 38% globally, followed by a significant decline in AIDS-related deaths.

As previously discussed, pregnant women with HIV infection are usually disgraced, stigmatized, and discriminated because of their condition. However, gestation represents the highest personal and social value that should be protected and preserved. It is, therefore, society’s responsibility to identify and eliminate biases, not only in the general population, but also in clinical settings, so that all sick individuals are respected and cared for, regardless of race, religion, gender, nationality, or condition. 36 – 38 The ideal approach to enforcing social support is to envision it as having both a practical and an emotional dimension. Emotional support plays an extremely important role in the lives of these people suffering from long-term diseases. The significance of emotional support is evident in studies that show a strong correlation between lack of support even between people with normal mental state. 25 , 27 , 39 – 41

QoL refers to the personal satisfaction expressed or experienced by individuals regarding their physical, mental, and social status. It can be defined as a multidimensional notion that involves a satisfactory social status and role, physical well-being, intellectual functioning in a stable, healthy, emotional environment, as well as a grounded self-esteem. 42 People living with AIDS are discredited, considering their lives so diminished that they no longer that life is worth living. Thus, the ethical task is to figure out how to approach this growing sociomedical issue. The medical profession is the area where the problem is most evident, and it is an area requiring special learning and training, based on oaths and codes of ethics. Since women remain unaware about AIDS and its spectrum, it is our responsibility as doctors to concern ourselves with improving their QoL. 43 – 46

The role of medicine

The medical profession has traditionally (and inaccurately) reinforced a gender stereotype by looking upon women as the weaker sex in biological terms. 6 This approach should be corrected, and various support programs should be structured and introduced in such a way so as to mobilize and inspire the entire society, and especially the young people, to build a new, more humane society that will respect all human beings. Governments and medical professionals should provide all the necessary resources and guidance and commit themselves to supporting HIV-positive women, combat ignorance and stigmatization, and reduce the widespread poverty that accompanies their condition. Besides access to multidisciplinary, interdisciplinary, and participatory programs and the strengthening of basic health care, government officials should go beyond medical science. They should investigate the denigration of women worldwide, as well as the economic disintegration in many countries that prevents childbearing women from getting adequate infrastructure and effective antiretroviral therapies. 47 – 51

Confidentiality of medical information

The sensitive personal information disclosed by the patient to a physician may frequently be of interest to parties outside the medical profession. However, this information has been traditionally, ethically, and legally guarded by confidentiality. Medical ethics bases this duty on the obligation to respect the patient’s privacy and autonomy, as well as on the need for loyalty and trust on the part of the physician. 52 Nevertheless, confidentiality has been treated rather superficially and carelessly in modern medical practice. It is true that computerization of medical records enhances statistical analysis and facilitates administrative tasks. However, nowadays, with all the technological progress, malevolent and unauthorized personnel are allowed to have access and reveal medical information. Confidentiality is undoubtedly an unwritten ethical obligation. Physicians who carry the responsibility to protect their patients must be familiar with the regulations and policies so as to safeguard the patient’s medical information. Prevention is better than cure; therefore, expert advice, support, and education should be provided to safeguard medical identity. 44 , 46 , 53 – 57

Current international approach and results

Lack of a clearly defined approach of stigma prevents experienced personnel from introducing efficient treatment programs and new initiatives with the final aim of annihilating discrimination. The stigma carries the inherent identity of dividing people into groups.

Literature reveals numerous survey methodologies and interviews of people living with AIDS or of the general population, both emphasizing their experience of HIV stigma, on access to prevention, treatment, and care, with a very small part of the articles referring to the need to create valid and reliable measures on evaluating the stigma through psychological tests and methods to eliminate it. 58 – 60 However, due to the nature of the aforementioned social stigma, evaluating and practical measuring of the multifaceted stigma have proven to be significantly difficult. It is evident and profound that not many methods have been introduced into health care systems for a direct measurement of the HIV-related stigma and its cognate parameters. Since socioeconomical issues are the main predisposing factors of low educational level and lack of university/social program funding, these methods are marginalized. The economic difficulties complicate data collection of the infected population, the governments avoid investing in the appropriate information of the citizens, and lack of adequate health support is dominating. 58 – 60

The global HIV–AIDS response reported a great rise of the people infected with AIDS in the last few years, but a reduction of the newly infected and the people dying from HIV. 61 This has to do not only with the new facilities providing therapy and the more people receiving it but also due to the increased information on the issue of pregnant women with HIV. Therefore, more women are tested and eventually receive therapy to avoid mother-to-child transition. These are the results of the difficult efforts of World Health Organization, United Nations Children’s Fund, and The Joint United Nations Programme on HIV/AIDS, in collaboration with national and international partners, to monitor key components of the health sector response to the HIV epidemic. 61

The basis of mass-media interventions is one of the main solutions on reducing stigma. The design of stigma elimination methods relies on behavior and social attitude. Electronic mass communication media, aimed at a wide audience, is a very efficient means of introducing new ideas, beliefs, and updated knowledge on AIDS through continuous and repetitive electronic messages. Digital technology and cultural exposure combined with the subject’s personal experiences can have a significant effect on people and society itself.

Prevention and possible solutions to eliminate the HIV stigma

The first and undisputable step in HIV prevention is the introduction of the childbearer’s HIV testing. Many subjects do not join group testing due to the fear of stigmatization and family rejection while the problem is promoted by the everlasting stigma. Infected people might feel inferior to others if it is disclosed that they have tested positive, they are inherently fragile, prone to panic and run, a dangerous situation not so much because of the damage they do to individuals, but due to being vulnerable to explosive emotions of anger, depression and anxiety that lead them to negative thoughts. The problem ends up being a vicious cycle. 62 – 64

In a world of changing societies, increasing poverty problems, governmental conflicts, inequality as main parts of the main social problems, the HIV–AIDS stigma remains rooted. Although the main reasons for this stigma remain unclear, it is commonly accepted that they originate from within the core of society. The social stigma is a pervasive problem regarding the attempts of HIV prevention, diagnosis, and treatment. The social stigma is a pervasive problem regarding the attempts of HIV prevention, diagnosis, and treatment. People need to have access to prognosis, diagnosis, and treatment. The government, in accordance with institutions and communities, needs to create programs involving contacting people, providing legal interventions, training programs, self-help and support groups, homecare teams, rehabilitation programs, and educational projects so as not only to accept and help people living with AIDS but also to spread the idea of prevention. Assessment of the stigma elimination within a social group suggests the allocation of projects and the use of reliable parameters and mechanisms within the affected groups. Literacy is of vital importance in the battle against HIV–AIDS stigma annihilation. The presentation of facts on AIDS is a good start. It is important to take into consideration the fact that such research programs are limited by the small size of samples. Social lives are devastated and patients avoid participating in research projects. A new generation of analysts, an exceptional network of policymakers, thinkers, leaders, and scholars who fully acknowledge the range of the stigma, needs to be recruited to reverse this phenomenon. In addition, nongovernmental organizations, philanthropic groups, and individual donors, with the help of digital technology and media, interested in the future of our society need to have the appropriate support for their valuable effort of eliminating the stigma. 58

The need for adequate public health care

The principle that human beings are entitled to adequate health care is found in various international documents. These reports focus on the role of nondiscrimination attitudes and behaviors in propagating and shielding the right to protect oneself against malnutrition, extreme weather conditions, and lack of basic health care conditions that could potentially cause high morbidity and mortality rates; it is a matter of life and death. 7 – 9

An inadequate standard of living is a threat to people with an immunocompromising comorbidity, such as HIV infection. A person with AIDS who lacks decent shelter, clothing, food, especially due to lack of health care access, will definitely face more difficulty even common diseases. Although health care is considered to be a basic human right in a civilized society, a good number of infected women live in poverty, experiencing high levels of stress caused by fatigue, fear, and lack of self-esteem, and have minimal access to the most fundamental health care services guaranteed and secured by every nation’s constitution. As a result, stigmatized women report depression, irritability, insomnia, and nervousness; it is a cluster of factors that creates extreme tension. 11 , 13 – 14

As we have already discussed, mental health is the core of a healthy self-esteem. However, segregation, isolation, and other restrictions attached to the HIV status may trigger unjustified soaring discrimination. Combined with other stigmatizing conditions, several negative characteristics are attributed to pregnant women with HIV. These women are improperly blamed as the main hosts and the basic transmitters of the virus to other people and their children. Public health is the result of collaboration between society and science on preventing disease and promoting health and safety for people, guided by epidemiological data. 65 However, the systematic maltreatment of women, in addition to slaughter and banishment of ethnic groups in Eastern Europe and Africa, demonstrates the abuse of human rights and the difficulty for public health to predominate. Medico-legal experts should focus on self-knowledge, self-improvement, social reform, and peace of mind. 7 – 11

Stigma has a very true historical foundation. The increasing fragility of the social bonding has destabilized the social structure. All diseases possess a certain degree of a potentially active social stigma, which threatens social and personal interactions. In Western societies, where individual effort and achievement are highly valued, people suffering from permanent disabilities are frequently less likely to succeed, isolated in a dependent and weak position, and criminalized and negatively evaluated. 66 For example, different types of physical deformities denote weakness in a world where physical strength and appearance are glorified. Being sick is both an individual experience and a social norm. Patients experience panic, discomfort, disorientation, and marginalization. The HIV-AIDS pandemic has caused enormous suffering throughout the world and presents a major challenge to society. It is society’s duty to accurately follow the development of the citizens, put an end to suffering, and eventually allow women to reengage organized social groups and structures. In times of rapid changes, where the world is more predictable than usual, subjects and organizations should be given the ability to innovate. One basic axiom should govern allowance of flexibility, instead of constraint enforcement. A radical societal reshaping will ultimately protect the vulnerable.

As it was previously discussed, stigma devalues and diminishes the dignity of people who are subjected to it. Although HIV-AIDS has only been around for 40 years, its stigma is prominent and needs to be addressed and corrected, since the inevitable social consequences of being stigmatized lead to severely reduced opportunities, discrimination, and even rejection. One of the tragic consequences of discrimination is that it has a deep impact on vulnerable and sensitive groups. Discrimination against women in male-dominated societies can fundamentally threaten their social, economic, and family positions. Unfortunately, not too much progress has been made in annihilating the stigma throughout the years. Some years into the epidemic with no effective vaccine or permanent HIV cure, no solution has been given to the affected pregnant women that end up isolated. Discrimination and rejection guide people’s lives, associating this stigma with prolonged and severe psychological trauma. Stigma and discrimination are strong parameters in creating a hidden society that is extremely difficult to reach and reveal – a society governed by its own unique rules. Although striking differences in culture, mentality, social perspectives, language, and history of human rights exist within the societies, a total front should be created against the AIDS pandemic. Governments should review existing laws and enforce new ones that will repeal these legal frames that support discrimination.

The value of personal autonomy is deeply ingrained in our civilization; it is the intrinsic moral right of a person to follow their own plan, thoughts, and goals in life. The fight against HIV-AIDS should, therefore, aim towards women’s empowerment and decisive moves for solutions by society. Society should dare to attempt a shift in strategy with or without support from the governments. Only then, the stigma will be eliminated. HIV-positive women must be embraced as respected and indispensable members of our society.

Acknowledgments

We would like to thank all residents and staff at Democritus University of Thrace - Department of Medicine.

The authors report no conflicts of interest in this work.

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There’s a New Covid Variant. What Will That Mean for Spring and Summer?

Experts are closely watching KP.2, now the leading variant.

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By Dani Blum

For most of this year, the JN.1 variant of the coronavirus accounted for an overwhelming majority of Covid cases . But now, an offshoot variant called KP.2 is taking off. The variant, which made up just one percent of cases in the United States in mid-March, now makes up over a quarter.

KP.2 belongs to a subset of Covid variants that scientists have cheekily nicknamed “FLiRT,” drawn from the letters in the names of their mutations. They are descendants of JN.1, and KP.2 is “very, very close” to JN.1, said Dr. David Ho, a virologist at Columbia University. But Dr. Ho has conducted early lab tests in cells that suggest that slight differences in KP.2’s spike protein might make it better at evading our immune defenses and slightly more infectious than JN.1.

While cases currently don’t appear to be on the rise, researchers and physicians are closely watching whether the variant will drive a summer surge.

“I don’t think anybody’s expecting things to change abruptly, necessarily,” said Dr. Marc Sala, co-director of the Northwestern Medicine Comprehensive Covid-19 Center in Chicago. But KP.2 will most likely “be our new norm,’” he said. Here’s what to know.

The current spread of Covid

Experts said it would take several weeks to see whether KP.2 might lead to a rise in Covid cases, and noted that we have only a limited understanding of how the virus is spreading. Since the public health emergency ended , there is less robust data available on cases, and doctors said fewer people were using Covid tests.

But what we do know is reassuring: Despite the shift in variants, data from the C.D.C. suggests there are only “minimal ” levels of the virus circulating in wastewater nationally, and emergency department visits and hospitalizations fell between early March and late April.

“I don’t want to say that we already know everything about KP.2,” said Dr. Ziyad Al-Aly, the chief of research and development at the Veterans Affairs St. Louis Healthcare System. “But at this time, I’m not seeing any major indications of anything ominous.”

Protection from vaccines and past infections

Experts said that even if you had JN.1, you may still get reinfected with KP.2 — particularly if it’s been several months or longer since your last bout of Covid.

KP.2 could infect even people who got the most updated vaccine, Dr. Ho said, since that shot targets XBB.1.5, a variant that is notably different from JN.1 and its descendants. An early version of a paper released in April by researchers in Japan suggested that KP.2 might be more adept than JN.1 at infecting people who received the most recent Covid vaccine. (The research has not yet been peer-reviewed or published.) A spokesperson for the C.D.C. said the agency was continuing to monitor how vaccines perform against KP.2.

Still, the shot does provide some protection, especially against severe disease, doctors said, as do previous infections. At this point, there isn’t reason to believe that KP.2 would cause more severe illness than other strains, the C.D.C. spokesperson said. But people who are 65 and older, pregnant or immunocompromised remain at higher risk of serious complications from Covid.

Those groups, in particular, may want to get the updated vaccine if they haven’t yet, said Dr. Peter Chin-Hong, an infectious disease specialist at the University of California, San Francisco. The C.D.C. has recommended t hat people 65 and older who already received one dose of the updated vaccine get an additional shot at least four months later.

“Even though it’s the lowest level of deaths and hospitalizations we’ve seen, I’m still taking care of sick people with Covid,” he said. “And they all have one unifying theme, which is that they’re older and they didn’t get the latest shot.”

The latest on symptoms and long Covid

Doctors said that the symptoms of both KP.2 and JN.1 — which now makes up around 16 percent of cases — are most likely similar to those seen with other variants . These include sore throat, runny nose, coughing, head and body aches, fever, congestion, fatigue and in severe cases, shortness of breath. Fewer people lose their sense of taste and smell now than did at the start of the pandemic, but some people will still experience those symptoms.

Dr. Chin-Hong said that patients were often surprised that diarrhea, nausea and vomiting could be Covid symptoms as well, and that they sometimes confused those issues as signs that they had norovirus .

For many people who’ve already had Covid, a reinfection is often as mild or milder than their first case. While new cases of long Covid are less common now than they were at the start of the pandemic, repeat infections do raise the risk of developing long Covid, said Fikadu Tafesse, a virologist at Oregon Health & Science University. But researchers are still trying to determine by how much — one of many issues scientists are trying to untangle as the pandemic continues to evolve.

“That’s the nature of the virus,” Dr. Tafesse said. “It keeps mutating.”

Dani Blum is a health reporter for The Times. More about Dani Blum