HIV/AIDS

Human immunodeficiency virus (HIV) is a lentivirus, a type of retrovirus, that infects CD4-positive T cells and other immune cells and gradually weakens the immune system. Untreated infection usually progresses over years to acquired immunodeficiency syndrome (AIDS), the stage defined by severe immune depletion and by opportunistic infections or cancers. Infection is lifelong, but modern antiretroviral therapy can suppress the virus to undetectable levels, so that people living with HIV can live nearly normal lifespans and can no longer sexually transmit the virus.

HIV is one of the most consequential infectious diseases in modern history. Since the epidemic was first recognized in 1981, it has killed tens of millions of people and reshaped public health policy, medical research, and the global response to infectious disease. UNAIDS estimates that about 41.0 million people were living with HIV in 2025, that 1.2 million people acquired the virus that year, and that 570,000 died of AIDS-related illnesses, while 32.1 million people were accessing antiretroviral therapy. These figures make the epidemic a central case in epidemiology, vaccine research, and debates about access to medicines.

This entry covers how HIV was discovered and where it came from, the structure and replication of the virus, the course of infection and its effects on the immune system, transmission and diagnosis, treatment and prevention, research toward a vaccine and a cure, and the global epidemiology of the disease. It ends with the social, legal, and institutional dimensions of the epidemic, including stigma, human rights, and the funding and governance of the global response.

Discovery and naming of the disease

The first published description came from the U.S. Centers for Disease Control and Prevention (CDC). Its June 4, 1981, MMWR report described five young men, all active homosexuals, treated for biopsy-confirmed Pneumocystis carinii pneumonia at three hospitals in Los Angeles. The patients were otherwise healthy, and the infection was one that almost never affected people with intact immune systems. The same year, the CDC also reported Kaposi's sarcoma and Pneumocystis pneumonia among homosexual men in New York City and California. The report reached clinicians four months before the first peer-reviewed article on the syndrome, and within a week the CDC received numerous reports of similar cases. By the end of 1981, 270 cases of severe immune deficiency among gay men had been reported, and 121 of those individuals had died.

The name took longer to settle. Because the cases were concentrated among gay men, the CDC first named the disease GRID, an acronym for Gay Related Immune Deficiency. That label was dropped as cases appeared in other groups, including injection drug users, hemophiliacs, and heterosexual partners. The CDC began using the term AIDS in September 1982 and issued its first case definition at the same time, a point on which some sources give slightly different dates. Even after transmission routes were identified, the stigma attached to the early label proved durable. By 1983 the CDC had identified all major routes of transmission and that female partners of AIDS-positive men could be infected, yet the public still considered AIDS a gay disease.

Identifying the cause followed in 1983. At the Pasteur Institute in Paris, Luc Montagnier's group, including Françoise Barré-Sinoussi, found a retrovirus in the lymphoid tissue of a patient with AIDS, which they called LAV. They published in May 1983. Montagnier sent samples to Robert Gallo at the U.S. National Cancer Institute, where by December Gallo's lab was successfully cultivating LAV. Gallo then published papers claiming that AIDS was caused by a related retrovirus he called HTLV-III. On April 23, 1984, a U.S. health secretary announced at a press conference, with Gallo, that Gallo's group had isolated the cause of AIDS, a claim made in Montagnier's absence.

The two laboratories then disputed priority. Much of the dispute concerned royalties from a forthcoming blood test. In 1987 the president of the United States and the prime minister of France announced a joint agreement declaring that Gallo and Montagnier shared credit for the discovery, and that the two governments would share patent royalties. Later investigations found that the U.S. laboratory strain had been derived from a French isolate that had contaminated another culture, although they did not conclude that Gallo had deliberately taken the virus. By 2002 the rivals publicly agreed that Montagnier's team had discovered HIV, while Gallo's team had first shown its role in AIDS. The virus received its present name in 1986, when both the French name LAV and the U.S. name HTLV-III were dropped in favour of HIV.

Recognition was formalized in 2008, when the Nobel Prize in Physiology or Medicine was shared by Barré-Sinoussi and Montagnier for the discovery of HIV, while Gallo was not included. Controversy flared again that year because Gallo's contribution was overlooked.

Early perceptions of the disease were shaped by limited knowledge. Diagnostic tests did not exist until the mid-1980s, and no effective treatment was available for many years, so the disease was often seen as a fatal condition affecting specific social groups rather than as a viral infection with a broad population risk. These early assumptions, together with stigma against gay men and people who injected drugs, influenced public policy, research funding, and clinical responses for years afterward.

Origins and evolutionary history

HIV's ancestry lies in simian immunodeficiency viruses (SIV) that infect African primates. HIV-1 and HIV-2 did not come from a single event: HIV/AIDS results from at least eleven cross-species transmission events of simian immunodeficiency virus from non-human African primates to humans. Three of these transfers, from chimpanzees, produced HIV-1 groups M, N and O, while the other eight came from sooty mangabeys and gave rise to HIV-2 groups A through H (the eight SIVsm transmissions from sooty mangabeys gave rise to HIV-2 groups A through H). The chimpanzee viruses were themselves hybrids: SIVcpz is a recombinant between two SIV lineages from old world monkeys. Recombination among viruses in chimpanzees appears to have supplied the genetic changes that later helped the virus adapt to human hosts, including the acquisition of a functional vif gene (key events preceding the emergence of pandemic HIV-1 group M strains were the recombination of different SIVs in chimpanzees).

HIV-1 is divided into four phylogenetic lineages, groups M, N, O, and P, each of which resulted from an independent cross-species transmission event of simian immunodeficiency viruses infecting African apes. Group M is by far the largest: it accounts for over 95% of global infections. Its immediate source has been traced to a particular chimpanzee population. Chimpanzee viruses from the central subspecies have been traced as the original source of HIV-1 group M, and the closely related reservoir has been located in rural south-east Cameroon. Group N also descends from chimpanzee viruses in the same region. The origins of groups O and P are less settled. A 2015 study argued that the remaining two groups also emerged in southern Cameroon but had their origins in western lowland gorillas. Other analyses have judged the source of these groups to be still unclear, leaving open whether gorillas were the direct source or whether chimpanzees acted as an intermediate host.

Molecular dating indicates that the lineage behind the pandemic emerged only a little over a century ago. Estimates vary with the dataset and the method. A 2020 analysis of a 1966 genome from Kinshasa placed the origin of the pandemic lineage of HIV-1 to a time period around the turn of the 20th century (1881 to 1918). Other studies put the common ancestor of group M around the 1920s in central Africa, and a 2010s-era analysis of genomes reported an estimated mean time to the most recent common ancestor of 1922. Direct evidence is limited but consistent with this picture. An archival plasma sample from 1959 pinpointed the infection to the area around what is now Kinshasa in the Democratic Republic of Congo. Because the common ancestor predates the virus's wider spread by only a few decades, the initial cross-species event is thought to have occurred in the late nineteenth or early twentieth century (the cross-species transmission of SIVcpz giving rise to HIV-1 group M must have been in late 19th–early 20th century).

Why the virus became epidemic at that time, rather than earlier, remains a matter of hypothesis. Zoonotic spillovers were probably not rare in the past: the opportunities for chimpanzee- or monkey-to-human host jumps have existed for hundreds or thousands of years, yet the virus only became detectable in human populations in the twentieth century. Researchers therefore point to social and environmental changes. Proposed contributors include ape hunting, social disruption, commercial sex work, sexually transmitted infections, and travel toward Kinshasa in the period 1899–1923 (the region had intense ape hunting, social disruption, commercial sex work, STDs, and traffic to/from Kinshasa in the period 1899–1923). Urban growth and transport routes are also considered significant, since reconstructing the early dynamics of the pandemic can illuminate the roles of urbanization and transportation networks. Rivers were a major route as well: the rivers from southeast Cameroon flow south, ultimately joining the Congo River on which Kinshasa is located. Medical practices have also been examined. Injection treatments became more common around 1930, but their frequency among local patients was far lower than in modern parenteral HIV outbreaks, so they are considered at most a partial explanation.

Virus structure and genetic diversity

HIV is an enveloped virus whose RNA genome encodes the structural proteins Gag, Pol and Env, along with regulatory proteins such as Tat and Rev and several accessory proteins. Env is made as one long precursor. Cellular furin cuts it into two subunits, the outer gp120 and the membrane-anchored gp41, and the two glycoproteins are organized into trimeric complexes on the virion surface. These spikes are the only viral proteins exposed on the particle's surface, which makes them the main point of contact with both host cells and the immune system.

The envelope works in two steps during entry. Binding of the initial receptor, CD4, induces changes in gp120 conformation that allow high-affinity interaction with the coreceptor, CCR5 or CXCR4. The gp41 subunit then changes shape, and the resulting six-helix bundle coincides with the fusion of the viral and cell membranes. The same surface that enables entry is also the target of antibodies. gp120 is a primary target of the humoral immune response, and it has evolved to resist antibody-mediated neutralization. Much of that resistance lies in its variable segments. gp120 is built from conserved regions interspersed with five variable regions (V1–V5), and in the structures solved so far these variable segments form loops that protrude from a conserved core. Loop variation, shielding by sugars, and conformational shifts together hide conserved sites from antibodies.

The main engine of diversity is the viral reverse transcriptase, an enzyme that copies the RNA genome into DNA. Because it lacks proofreading activity and has an estimated error rate on the order of 3 × 10^−5 per base per round of copying as determined in cell culture studies. Other estimates are considerably higher, with mutations due to uncorrected RT activity appearing at a rate of about 1 in every 1500–4000 nucleotides per replication cycle. Given a genome of about 9,200 bases, the higher figure implies roughly two to six errors per genome in each cycle, by my own arithmetic. Measurements in patients show even more change. One study of viral DNA in infected people found one mutation every 250 bases. Most of that excess does not come from the polymerase. The same analysis reported that the HIV-1 reverse transcriptase contributes only 2% of mutations, whereas 98% result from editing by host cytidine deaminases of the A3 family. These host enzymes are carried into new cells inside the virus particle, which means that host defenses also add mutations during infection. Recombination adds a further layer. Because the enzyme often switches templates during copying, high recombination rates observed in retroviruses are promoted by poor processivity that causes template switching.

Within a single infected person, these processes produce a large, rapidly changing population of related viruses. The rapid turnover, high mutation rate, and high frequency of recombination result in a diverse viral population. This variation is the basis for mutation-driven drug resistance. When a drug suppresses one set of variants, others that carry changes at the drug's target can persist and expand. The same variation enables immune escape. The reverse transcriptase is responsible for much of the antigenic variation of HIV that confounds both the natural immune response and vaccine development, although the in vivo data suggest that host editing may account for a larger share than the enzyme itself. Because the population contains many antigenically distinct forms, a single vaccine that protects against all of them remains difficult to design. The same diversity also shows how natural selection acts quickly on a virus that replicates continuously in a single host.

Replication cycle

HIV enters cells by binding to CD4, a receptor on the surface of certain immune cells, and then to a second receptor called a coreceptor. The surface glycoprotein gp120 attaches to CD4, which changes its shape so that it can engage either CCR5 or CXCR4. Strains that use CCR5 (R5 viruses) predominate in early infection and transmission, while CXCR4-using (X4) strains are more often found in later disease. The gp41 subunit then drives fusion of the viral envelope with the cell membrane, releasing the viral core into the cytoplasm. The main targets are CD4 T cells, but macrophages and dendritic cells also carry the receptors, and dendritic cells can transport virus to lymphoid tissue.

Once the core is inside the host cell, it is uncoated and the viral reverse transcriptase copies the single-stranded RNA genome into DNA. The enzyme first synthesizes a complementary DNA strand, removes the RNA template, and then copies the second strand, producing linear double-stranded DNA with viral terminal repeats at each end. This DNA travels with viral proteins through the nuclear pore, which is why HIV can establish infection in cells that are not actively dividing. In the nucleus, the viral integrase cuts the host chromosome and inserts the viral DNA into it, creating a provirus. Integration is effectively permanent: the viral genome becomes part of the cell's own DNA and is copied whenever that cell divides.

Transcription of the provirus is carried out by the host's RNA polymerase, which starts at the viral promoter in the 5′ terminal repeat. The viral protein Tat greatly increases the efficiency of transcription by binding a structured RNA element at the start of the transcripts. Early transcripts are heavily spliced and encode Tat and Rev. Rev then allows unspliced and partly spliced RNAs, which encode the structural proteins, to leave the nucleus. Translation yields the Gag and Gag-Pol polyproteins, and the envelope glycoproteins are made from a separate spliced transcript. Gag and Gag-Pol assemble beneath the plasma membrane, with the genomic RNA and envelope proteins incorporated. The new particle buds out of the cell, taking a piece of host membrane with it. At this stage the virion is not yet infectious. The viral protease then cleaves the polyproteins into mature components, and only after this maturation step can the new particle infect another cell.

The cycle also explains why HIV is so difficult to eliminate. Some integrated proviruses enter a latent state, often in resting memory CD4 T cells, where transcription is very low and no new virions are made. Because these cells can survive for a long time, they form a reservoir that is not reached by drugs targeting active replication. Antiretroviral therapy works by interrupting steps of the cycle in cells that are actively producing virus, so it suppresses viral load but does not remove the integrated provirus. Interruption of treatment therefore usually leads to rebound from the reservoir, a central reason why current treatment must be continued long term and why drug development and cure research focus on the latent state.

Each stage of the cycle corresponds to a major class of antiretroviral drugs. Entry inhibitors block the interaction with CD4 or the coreceptor, or the fusion step. Nucleoside and non-nucleoside reverse transcriptase inhibitors interfere with DNA synthesis, integrase inhibitors block insertion into the host genome, and protease inhibitors prevent the production of mature infectious particles. Because the reverse transcriptase makes frequent errors and the cycle repeats many times a day in an infected person, combining drugs that act at different steps is necessary to limit resistance. Understanding the stages of the cycle is therefore the basis for both the design of treatment and the explanation of latency.

Pathogenesis and immune damage

Mechanisms of CD4 T-cell loss

The depletion of CD4 T cells is the defining feature of HIV disease, and the mechanism behind it has been debated for decades. Earlier ex vivo studies tended to implicate apoptosis as the main driver of CD4 death. Later work in infected macaques shifted this picture. Caspase-1-induced pyroptosis, a highly inflammatory form of programmed cell death, was identified as the dominant cause of rapid CD4 loss in gut-associated lymphoid tissue, spleen, and lymph nodes during acute infection. Caspase-3-mediated apoptosis and direct viral cytotoxicity accounted for only a small fraction of the deaths.

Most of the cells that die are not infected. In a 2022 preprint on acute SIV infection, the majority of CD4 T cell death (~95%) occurred in uninfected bystander cells, and pyroptosis was induced via innate immune sensing of incomplete reverse transcription products accumulated during abortive HIV-1 infection. Death also spreads through the tissue. Inflammatory molecules released by dying cells pull additional cells into the same fate, so this death pathway links the two signature events in HIV infection—CD4 T-cell depletion and chronic inflammation. A separate line of thinking holds that the principal mechanism of CD4 T-cell depletion by HIV is due to its use of CD4 as its primary receptor and the signaling induced through this receptor on nonpermissive (resting) T-lymphocytes.

Replacement of these cells is also impaired. The thymus produces fewer new T cells over time, and the lymphoid organs that house them become scarred, resulting in immune deficiency via increased infection of the T cells, low thymic output, lymphoid tissue fibrosis, and T and B cell dysfunction.

The gut as the epicentre

Across the course of disease, the largest CD4 deficits appear in the intestine, where CCR5-bearing cells are hit hardest. Early on, the virus rapidly removes memory helper populations, including Th17 and Th22 cells, that keep the gut lining intact. Gut permeability allows translocation of microbial products into the systemic circulation, causing systemic immune activation. This process, known as microbial translocation, is one of the main links between the damaged gut and the wider immune system. Once the barrier fails, bacterial products keep the inflammatory response switched on throughout the body.

Chronic immune activation

Viral load is a comparatively weak forecaster of how fast disease advances, and immune activation is considered at least as important. Even when antiretroviral therapy suppresses viral replication, immune activation persists and is predictive of disease progression. Persistent inflammation is also linked to some cancers, cardiovascular disease, and chronic kidney disease, which can appear even in people with good viral control.

Tissue reservoirs and the central nervous system

Early in infection, the virus seeds a durable pool in gut tissue, and treatment does not clear it. A stable viral reservoir is established in the gut very early in infection that is not eradicated even during long-term suppressive anti-retroviral therapy. The central nervous system shows a similar pattern. In macaque studies, treatment left viral genetic material in the frontal cortex and the intestine largely unchanged. Clinically, roughly two in five people on effective treatment still show some degree of HIV-associated neurocognitive disorder. Animal experiments also suggest the gut can drive this: when researchers injured the intestine of uninfected macaques, the brain showed inflammatory changes much like those in infected animals.

Loss of control over ordinary pathogens

As CD4 counts drop, the immune system loses its grip on organisms it normally keeps in check. Cell-mediated defenses against fungi, intracellular bacteria, and certain viruses weaken, so common microbes cause severe disease. Pneumocystis pneumonia, cryptococcal meningitis, tuberculosis, and cytomegalovirus disease become more frequent as the immunodeficiency deepens, and the conventional threshold of about 200 CD4 cells per cubic millimetre marks the point where these infections become a major risk.

Clinical course and staging

Acute infection

Acute retroviral syndrome usually appears about two to four weeks after exposure, when the virus is multiplying rapidly and spreading through lymphoid tissue. Many people, though not all, develop fever, rash, sore throat, fatigue, muscle aches, and swollen lymph nodes. These signs are nonspecific, so they are often attributed to influenza, infectious mononucleosis, or another common viral illness, and the infection frequently goes unrecognized. Plasma viral load is very high at this stage, and CD4 T cells, particularly in the gut mucosa, are depleted quickly. Standard antibody tests may still be negative, so diagnosis during this window relies on detecting viral RNA or antigen (see diagnosis).

As the adaptive immune response develops, viral load falls to a lower level, known as the viral set point, and the acute symptoms usually resolve within a few weeks.

Clinical latency

After this phase, many people enter a long period with few or no symptoms, which can last for years. The term "latency" can be misleading, because the virus is not dormant. Replication continues at a low level, mainly in lymphoid tissue, and the immune system gradually loses CD4 T cells faster than the body can replace them. Some people develop persistent generalized lymphadenopathy, recurrent oral thrush, or herpes zoster during this stage, and these are recognized as early signs of advancing immune suppression.

Staging systems

The CDC and the WHO use CD4 counts and clinical events to classify disease. CD4 cells are counted by flow cytometry, and normal counts are typically above 500 cells/µL. In the CDC system, a count of 500 cells/µL or more (or 29% of lymphocytes) corresponds to stage 1, a count of 200 to 499 cells/µL to stage 2, and a count below 200 cells/µL (or below 14% of lymphocytes) to stage 3, which is the AIDS stage. A diagnosis of AIDS can also be made at any CD4 level if a person develops an AIDS-defining condition. These conditions include Pneumocystis pneumonia, caused by a fungus; Kaposi sarcoma, a cancer associated with human herpesvirus 8; pulmonary tuberculosis, caused by a bacterium; cryptococcal meningitis; and esophageal candidiasis. The WHO clinical staging system instead ranks disease from stage 1 (asymptomatic) to stage 4 (severe illness) according to visible clinical conditions, and it uses CD4 counts to guide treatment eligibility.

Untreated course

Without antiretroviral treatment, median survival after infection has historically been about ten years, based largely on cohort studies from high-income countries before effective therapy existed. The range is wide. Older age at infection, coinfections such as tuberculosis or hepatitis, high viral load, and host genetic factors can shorten the interval, while a small group of people, sometimes called long-term non-progressors, have remained clinically stable for many years. Once CD4 counts fall below about 200 cells/µL, the risk of opportunistic infections and death rises steeply. Antiretroviral therapy, discussed below, has largely prevented this progression wherever it is available.

Transmission and risk

HIV is spread through a limited set of body fluids. Blood, semen (including pre-seminal fluid), rectal fluid, vaginal fluid and breast milk are the fluids generally regarded as able to carry enough virus to infect another person. Transmission needs three things at once: a fluid with enough virus, a route that lets it reach the bloodstream of an HIV-negative person, and an activity that brings the two together. The routes are mucous membranes, such as the lining of the rectum, vagina, penis opening or mouth, or broken skin. Fluid can also enter the bloodstream directly through a needle or syringe.

Main routes

Most infections worldwide arise from condomless vaginal or anal sex and from sharing needles or syringes among people who inject drugs. Among sexual practices, receptive anal intercourse carries the highest risk per act, while oral sex is considered a much less common route. Mother-to-child transmission can occur during pregnancy, during labour and delivery, or through breastfeeding. Transfusion of unscreened blood was once a major route, but screening of donated blood has largely eliminated it in well-resourced health systems. Needlestick injuries are a recognized but uncommon occupational exposure in health care.

Biological cofactors

The probability of transmission during a single exposure varies. The most important factor is the viral load of the partner living with HIV: the more virus present in the infected fluid, the greater the chance of infection. The presence of other sexually transmitted infections in either partner also raises the risk of sexual transmission, since inflammation and genital lesions can make infection more likely. The type of exposure matters as well, including the surface involved, whether tissue is damaged, and the amount of fluid that reaches the body.

Viral suppression and risk

Antiretroviral therapy has changed the risk picture in a fundamental way. Early studies, including a 2000 analysis of heterosexual couples in Uganda, found that partners with very low viral loads did not transmit the virus. The randomized HPTN 052 trial, which followed 1,763 serodiscordant couples, recorded no linked transmission when the partner living with HIV was virally suppressed. Later studies, such as PARTNER and Opposites Attract, extended this finding to male couples and transgender partners. A 2023 systematic review in The Lancet found no sexual transmission at viral loads below 600 copies/mL and exceedingly rare transmission below 1,000 copies/mL. Public health campaigns summarize this evidence as "Undetectable equals Untransmittable" (U=U), with 200 copies/mL commonly used as the practical threshold. The protection depends on sustained suppression, not merely on starting treatment. The evidence for sexual transmission is stronger than the evidence for needle-sharing transmission: antiretroviral therapy greatly reduces risk in that setting, but research has not established that an undetectable viral load eliminates it.

Non-transmission and myths

HIV does not spread through casual contact such as hugging, shaking hands, sharing dishes or using toilet seats. Saliva, tears, sweat, urine and feces do not transmit the virus unless they are visibly contaminated with blood. Closed-mouth kissing is not a meaningful route, and open-mouth kissing is highly unlikely to transmit HIV unless both partners have bleeding mouth sores. Mosquitoes and other insects cannot transmit HIV: the virus does not replicate in them, and a mosquito does not inject the blood of a previous host when it bites. HIV also survives poorly outside the body, which makes environmental transmission remote. These conclusions rest on decades of epidemiological observation and laboratory study, and they are widely accepted by public health authorities.

Structural factors

Biological risk does not fall evenly across populations. Poverty, gender inequality, sexual violence, stigma, criminalization of key populations and limited access to testing, condoms, clean injection equipment and treatment shape who is exposed and how long infection goes undetected. Women and girls in many settings have limited ability to negotiate condom use, and economic dependence can increase exposure. Sex workers, men who have sex with men, transgender people and people who inject drugs often face higher risk because of legal and social marginalization, not because of differences in behaviour alone. For this reason, social determinants of health and income inequality help explain why people with similar biological exposure experience very different levels of infection risk.

Diagnosis and monitoring

Laboratory screening

Routine laboratory screening now uses fourth-generation immunoassays that look for both HIV antibodies and the p24 antigen, a viral protein that is produced in large amounts early in infection, often before antibodies appear. Adding p24 detection narrows the window period. A 2024 study of primary-infection samples found that a fourth-generation rapid test shortened the diagnostic window from roughly three months to about one month, whereas antibody-only rapid tests performed poorly in the first weeks, with sensitivities in primary infection reported as low as 70%. Current UK guidance treats a negative fourth-generation laboratory result at 45 days after exposure as a reliable exclusion. Nucleic acid tests, which detect viral rna by PCR-based methods, can identify infection even earlier, but they are costlier and are usually reserved for acute infection or specific clinical situations rather than routine screening.

Rapid tests and self-testing

Rapid tests and self-test kits extend screening beyond clinics, which helps people reach testing who might otherwise avoid it. Because their sensitivity can be lower, especially soon after exposure, a reactive result must be followed by confirmatory laboratory testing before a diagnosis is made, and a non-reactive result obtained very early may need to be repeated once the window period has passed.

Viral load and CD4 monitoring

After diagnosis, the viral load, meaning the concentration of HIV RNA in plasma, is the main measure of how well treatment is working. The WHO moved toward viral load as the preferred monitoring approach in 2013 and recommended it for all people on treatment in 2016, with CD4 counts playing a secondary role. Under the US guidelines, viral load is measured at entry into care, at treatment initiation, and regularly afterwards; during initial treatment it is repeated every 4 to 8 weeks until it falls below the assay's detection limit, and every 3 months if suppression cannot be achieved. Australian guidance treats a result above 200 copies/mL as a sign of inadequate response and recommends repeat testing within 2 to 4 weeks, and no later than 8 weeks. Once suppression is sustained, testing intervals can be extended. In the US guidance, viral load may be checked every six months for people who have been suppressed for at least two years and whose CD4 counts are consistently above 300 cells/mm³.

CD4 counts, usually measured by flow-cytometry, quantify CD4 T cells and reflect immune status. They remain important for assessing immune recovery and for opportunistic infection risk. For people starting treatment, Australian guidance suggests testing every 3 to 4 months during the first two years when counts are below 300 cells/mm³, and every 6 months when they are at or above that level. For people with sustained suppression and high CD4 counts, testing can be reduced, and the US guidance advises against routine quarterly CD4 testing in patients with undetectable viral loads and counts above 200 cells/mm³. Children who are not yet on treatment have viral load and CD4 measured at diagnosis and then at least every 3 to 4 months.

Drug resistance testing

Resistance testing identifies mutations in the viral genome that reduce the effectiveness of specific drugs. A genotypic assay, which sequences viral genes, is the preferred method. Current US guidance recommends resistance testing for everyone starting treatment, to help select active drugs, but treatment should not be delayed while results are awaited. It is also used when virologic failure occurs, which is generally defined as persistent viral load above 200 copies/mL. The evidence for acting on the result is strongest when viral load exceeds 1,000 copies/mL. Testing should be done while the person is still taking the failing regimen or within four weeks of stopping it. Conventional resistance testing is not recommended when viral load is 200 copies/mL or lower, because benefit is unclear and assays often cannot be performed reliably at such low levels. Because resistance accumulates over time, clinicians interpret new results alongside previous treatment history and earlier test results.

Antiretroviral drugs and mechanisms

Antiretroviral drugs are grouped by the step of the viral life cycle they disrupt. Most current agents act on one of three viral enzymes, reverse transcriptase, integrase, or protease, while others block entry into the cell or interfere with the viral capsid. Because each class has a different target, the classes can be combined, and the mechanisms explain both how the drugs suppress replication and why resistance arises.

Reverse transcriptase inhibitors form the oldest group. Nucleoside reverse transcriptase inhibitors (NRTIs) are nucleoside analogues. After the host cell converts them into active triphosphate forms, the viral enzyme incorporates them into the growing DNA strand. Because they lack the chemical group needed to attach the next building block, the chain stops early. Nucleotide analogues (NtRTIs), such as tenofovir, work the same way but do not require the first phosphorylation step. Non-nucleoside reverse transcriptase inhibitors (NNRTIs) are structurally unrelated small molecules. They bind a hydrophobic pocket next to the enzyme's active site and distort it, so they never become part of the DNA. Because a single mutation in that pocket can weaken binding, NNRTIs as a class are especially vulnerable to resistance.

Protease inhibitors act late in the cycle. The virus produces long precursor polyproteins from the Gag and Gag-Pol genes, and the viral protease cuts them into functional pieces. Protease inhibitors block the enzyme's active site, so the particles that bud from the cell remain immature and non-infectious. Integrase strand transfer inhibitors (INSTIs), including raltegravir and dolutegravir, block the integrase enzyme at the step where it joins viral DNA to the host chromosome. This prevents the provirus from forming, so the drug stops infection at a point where the virus has already entered the cell.

Entry and attachment inhibitors act before the virus reaches the inside of the cell. Maraviroc is a CCR5 antagonist that binds the host coreceptor, so the viral envelope glycoprotein cannot use it. Because some viruses use CXCR4 instead, tropism testing is needed before use. Enfuvirtide is a fusion inhibitor that binds the gp41 subunit of the envelope and blocks fusion of viral and cell membranes; because it is a peptide, it is injected rather than taken by mouth. Fostemsavir, a CD4 attachment inhibitor, targets the gp120 subunit and has been approved for heavily treatment-experienced patients. Lenacapavir is a capsid inhibitor that binds the viral capsid protein and interferes with several stages of replication, including capsid assembly and nuclear entry. It is also the first drug in its class.

Long-acting injectable formulations have expanded the options for people who struggle with daily pills. Cabotegravir combined with rilpivirine, an integrase inhibitor and an NNRTI, was approved in the United States in 2021 for complete treatment and is given as injections every one to two months. Cabotegravir alone has been approved for pre-exposure prophylaxis. Lenacapavir, given as subcutaneous injections twice a year, was approved for multidrug-resistant HIV in 2022 and has since been approved for prevention. The World Health Organization recommended it as a PrEP option in 2025, and trials of combinations of long-acting agents continue.

Combination regimens are the standard approach because a virus must accumulate mutations against several drugs at once to escape all of them. Most regimens use a backbone of two NRTIs or NtRTIs together with a third agent from another class, or a two-drug regimen based on an integrase inhibitor. Drugs from the same class often share resistance pathways, so combining them offers little protection, and regimen design avoids this. Clinicians select agents based on several factors. Drug interactions matter, especially with enzyme-inducing or enzyme-inhibiting medicines, and rifampicin used to treat tuberculosis lowers the blood levels of several antiretrovirals. Side-effect profiles and the safety of each drug during pregnancy also influence choice. Tenofovir and emtricitabine are active against hepatitis B, so they are often preferred when this coinfection is present. Resistance testing before treatment and when treatment fails guides the final choice of drugs. This is the basis of the pharmacological approach used in modern clinical care.

Treatment history and clinical management

Zidovudine (AZT) was the first antiretroviral drug. It had been originally developed in the 1960s for cancer research, and the U.S. FDA's approval for HIV came in March 1987 (zidovudine (azidothymidine, AZT, ZDV) | Retrovir | March 19, 1987). Early placebo-controlled trials in people with advanced disease reported fewer opportunistic infections, higher CD4 counts and better survival over 24 weeks, but longer-term follow-up of this study failed to show a benefit of zidovudine over placebo. The drug could slow disease without controlling the virus. It helped people live longer, but it couldn't stop the virus from replicating when taken alone. Its toxicity also led researchers to develop safer dosage regimens.

The turning point came with combination therapy. In 1996, a regimen combining several drugs, including the newly developed class of protease inhibitors, became the standard of care in the United States. In the following year, AIDS-related deaths declined by 47%. The decline had begun earlier: the number of AIDS-related deaths in the U.S., which exceeded 40,000 in 1995, declined rapidly after the introduction of this combination therapy. A regional cohort in the United Kingdom recorded a 40% reduction in the death rate after combination therapy was introduced. Long-term analyses of patients starting antiretroviral therapy in Europe and North America found that all-cause mortality in the second and third years after starting ART declined substantially over calendar time. For many people, the condition became a chronic one rather than a rapidly fatal illness, and PAHO/WHO notes that life expectancy among people living with HIV is now comparable to that of the general population.

Treatment timing has also changed. In September 2015 the World Health Organization recommended treatment for all adults with HIV, regardless of WHO clinical stage and at any CD4 cell count, and the 2016 guidelines strongly recommended initiating ART for all adults living with HIV regardless of WHO clinical stage and at any CD4 cell count. This recommendation drew on a systematic review of three randomized trials (START, TEMPRANO and HPTN 052) and 17 observational studies. Current practice reflects this shift: the standard of care today is to initiate ART in nearly all people living with HIV, regardless of CD4 count. WHO guidance also calls for rapid starts, initiating ART within 7 days after HIV diagnosis, with same-day initiation where patients are ready. Exceptions exist. Immediate ART initiation is contraindicated among people living with HIV who may have central nervous system infections with risk of life-threatening IRIS, such as TB meningitis or cryptococcal meningitis.

Long-term clinical care focuses on several concerns. Adherence matters because regimens must be taken consistently to keep the virus suppressed and to prevent drug-resistant variants from emerging, and treatment is usually a combination of drugs from different classes. Drug toxicity has also shaped regimen choice: zidovudine is considered an alternative initial therapy in the World Health Organization (WHO) Guidelines but is no longer recommended in US guidelines because of toxicity. As patients age, comorbidities become more important, because as populations age, the risk of chronic conditions such as hypertension, diabetes, and other comorbidities increases. For this reason, PAHO/WHO recommends integrating noncommunicable diseases care into HIV service delivery. Cardiovascular and metabolic monitoring, therefore, forms part of routine care, and the goal has shifted from preventing early death to sustaining long-term quality of life.

Prevention

Prevention of HIV combines behavioural, biomedical and structural measures. Condoms, sterile injection equipment and harm-reduction programmes lower exposure in sexual and drug-use settings. Biomedical tools added to this base over the past two decades, including antiretroviral drugs used before and after exposure, and treatment that suppresses the virus in an infected person.

Pre-exposure and post-exposure prophylaxis

PrEP (pre-exposure prophylaxis) is the use of antiretroviral medication to prevent HIV. PrEP is for people without HIV who may be exposed to HIV through sex or injection drug use. The evidence base was built in stages. A 2013 Thai trial of daily oral tenofovir disoproxil fumarate showed that it reduced HIV acquisition among people who inject drugs, and CDC recommends that preexposure prophylaxis (PrEP) be considered as one of several prevention options for persons at very high risk for HIV acquisition through the injection of illicit drugs. Earlier randomized trials had already shown efficacy among men who have sex with men and among heterosexual men and women, although some trials failed, probably because of low adherence.

Adherence is the main determinant of protection. Protection from HIV will wane over 7-10 days after ceasing daily oral PrEP use. For vaginal exposure, the Panel recommends 20 days of oral PrEP before determining full protection from HIV acquisition via vaginal exposure. Long-acting injectables change this calculation. Once injections stop, drug levels decline gradually over a "tail period", during which resistance can develop if infection occurs, so clinicians counsel patients about this risk and plan a transition to daily oral PrEP when exposure continues.

Post-exposure prophylaxis (PEP) is an emergency measure rather than a routine one. PEP must be started within 72 hours (three days) after possible exposure to work effectively. The preferred regimens are taken for 28 days, and although PEP can help prevent HIV transmission, it should be used in emergencies only and is not meant for regular use by people who may be exposed to HIV frequently. A person who keeps facing exposure after a course may be moved onto PrEP.

Viral suppression as prevention

Effective treatment also prevents sexual transmission. The message "undetectable equals untransmittable" (U=U) summarises this. A person with HIV who maintains an undetectable viral load on treatment cannot pass the virus on through sex. The threshold used in practice is below 200 copies/ml of blood measured, and public health guidance has described the condition as achieved an undetectable viral load and maintains it for six months and thereafter. The scientific basis came from trials released in 2016: PARTNER and HPTN 052 reported that people with undetectable viral loads did not transmit HIV to HIV-negative partners through sex. The concept is an application of treatment as prevention, and it rests on large randomized trials rather than observational data alone.

Awareness of U=U is uneven. A 2024 meta-analysis found that U=U awareness was high among PLWH, moderate among MSM and healthcare professionals, and low in the general population. This gap matters because the message can reduce stigma and support testing, but only when people understand that it applies to effective treatment and sustained suppression.

Preventing mother-to-child transmission

Without intervention, the risk to infants is substantial. Transmission may occur during pregnancy, labour, delivery or breastfeeding, and without intervention rates can reach 15–45%. Mother-to-child transmission accounted for more than 90% of new childhood infections in earlier decades, and can be reduced to less than 5% by providing a HIV-positive mother access effective antiretroviral therapy (ART) and support services during pregnancy, delivery, and breastfeeding.

Current programmes rest on several linked steps. The first is testing, since mothers are tested for HIV as the first step in the EMTCT pathway. WHO guidance has moved toward initiation of life-long ART for all HIV-infected women, irrespective of their plasma viral load and CD4+ T cell counts, an approach known as Option B+. Infants also receive prophylaxis: the newborns of mothers living with HIV should receive 2 antiretroviral drugs (ARVs) for the first 6 weeks of life. Infant feeding is handled with care, because attempts to encourage women to abstain from all breastfeeding or to shorten the optimal duration of breastfeeding have led to increases in mortality among both uninfected and infected children. The preferred approach is to support breastfeeding while providing ART throughout.

Gaps remain. Expansion of maternal ART alone will not be sufficient to close the remaining gap and eliminate MTCT of HIV. Access to testing, treatment initiation and retention in care still vary widely between settings.

Vaccines and cure research

No HIV vaccine is currently licensed. The only vaccine trial to show efficacy so far is RV144, conducted in Thailand. Its protection was real but limited: it provided the first evidence that an HIV vaccine could give modest protection against acquisition (31.2% at 42 months of follow-up) in populations at low risk for infection. Its effect appeared stronger early on, with vaccine efficacy appearing higher (60%) at 12 months after vaccination, suggesting an early, but nondurable, effect. Because the trial was randomized and placebo-controlled, researchers have been able to study which immune responses tracked with protection. Later analyses found that protection correlated with antibodies to the V2 domain of gp120 and with high levels of antibody-dependent cellular cytotoxicity, but not with gp120-specific CD8+ T-cell responses. Some researchers have also argued that the vaccine's envelope proteins lacked certain sugar attachment sites that several families of broadly neutralizing antibodies require, which may have contributed to the limited efficacy.

The central obstacles to a vaccine are closely linked. Vaccine candidates tested in humans have not yet successfully generated strong bnAb responses against a wide spectrum of viruses. This is hard to solve because the envelope protein is highly variable, a direct consequence of the mutation-prone replication described in the earlier sections. A second obstacle is the latent reservoir. The reservoir sits in resting CD4+ T cells and myeloid cells at multiple locations in the body, including sanctuary sites such as the brain, and it is not cleared by antiretroviral therapy. Any cure strategy therefore has to deal with cells that are invisible to both drugs and the immune system.

The clearest evidence that HIV can be cured comes from a small number of transplant patients. The first, the so-called Berlin patient, was treated for leukemia with two allogeneic haematopoietic stem-cell transplantation (HSCT) procedures using a donor with a homozygous mutation in the HIV coreceptor CCR5 (CCR5Δ32/Δ32). Since then, a seventh individual, the "second Berlin Patient," has been reported as likely cured, joining six other individuals who were cured by a stem cell transplant to treat blood cancer and HIV. The London patient, treated for Hodgkin lymphoma, was also transplanted with CCR5-deficient donor cells. As of 2020, the London patient had been in HIV-1 remission for 30 months with no detectable replication-competent virus in blood, CSF, intestinal tissue, or lymphoid tissue. A later report described a patient whose donor carried only one copy of the CCR5 mutation, suggesting that the homozygous mutation may not be the only route to remission.

These cases do not translate into a general treatment. The procedures carry serious risks and are designed for people who already need transplantation for cancer. Conditioning chemotherapy and whole-body radiation were used to destroy the patient's malignant immune cells so that donor cells could rebuild an HIV-resistant immune system. Experts have stressed that even if CCR5-delta-32 stem cell transplantation can lead to a functional cure of HIV, this high-risk procedure will not be an option for most people. Gene-modified stem cells are being developed to reproduce the CCR5 effect without a matched donor, but that work remains experimental.

The "shock and kill" approach tries to reactivate latent proviruses so that the infected cells can be cleared by drugs or the immune system. Its aim is to activate latent proviruses in HIV-1 infected cells and subsequently kill these cells with strategies such as therapeutic vaccines or immune enhancement. Its limits are substantial. One review lists low inducibility of latency and limited efficacy when used alone as key drawbacks, and notes that combined approaches are in clinical trials. Genome editing aims to cut out integrated proviral DNA or to disable host receptors. In laboratory cell models, a CRISPR-based shock-and-kill system produced a modest 57.7% reduction in cells producing productive infection, along with only a 2.4-fold increase in cell death. In SIV-infected rhesus macaques, an AAV9-delivered CRISPR system reduced disease by removing integrated proviral DNA from blood cells and tissues, but delivery efficiency and long-term safety remain unresolved. A review of the field notes that the potential risks of transplantation and the low efficiency of current gene-editing methods have prevented the clinical achievement of an HIV cure. Therapeutic vaccines and broadly neutralizing antibodies are being studied as ways to strengthen the "kill" step, but all of these approaches remain experimental.

Global epidemiology and trends

UNAIDS estimated that 41.0 million people were living with HIV at the end of 2025, including 39.7 million adults and 1.3 million children under 15. The wide uncertainty interval around this figure, roughly 35.3 to 47.5 million, reflects that the numbers are modelled estimates built from data that 172 countries reported. In 2025 about 1.2 million people acquired HIV, and around 570,000 died of AIDS-related illnesses. Both annual figures are far below their historical peaks: new infections are about 65% lower than the 1994 peak, and AIDS deaths are about 73% lower than the 2004 peak.

Progress is real but uneven. Compared with 2010, new infections have fallen by about 42%, yet the decline has been too slow to meet the interim targets set for 2025, and UNAIDS warned that the world is well off track for the goal of fewer than 370,000 new infections a year. New infections rose in three regions and in 21 countries during 2025. Around 9 million people with HIV were still not receiving treatment, and nearly half of children living with HIV lacked access to antiretroviral therapy. WHO estimated that about 93,000 children acquired HIV in 2025, which is a sharp reduction from earlier years but still a substantial number.

The 95-95-95 framework sets out three benchmarks: 95% of people with HIV should know their status, 95% of those diagnosed should be on antiretroviral therapy, and 95% of those treated should have suppressed viral loads. Originally due by 2025, these targets were not met. UNAIDS data for 2025 show that 88% of people with HIV knew their status, 78% were on treatment, and 74% had a suppressed viral load. About 5.0 million people were unaware they were infected. WHO estimated that an additional 4.8 million people would need to be diagnosed, started on treatment, and suppressed to meet the third target. Member states reaffirmed the 95-95-95 targets in a 2026 United Nations political declaration, moving the deadline to 2030.

Women and girls form a large share of the epidemic, but the reported figure varies by source. UNAIDS reports that women and girls make up 53% of people living with HIV, while a U.S. government summary gives 51%. They accounted for 44% of new infections in 2025. Access gaps also differ by sex: UNAIDS reports that 84% of women aged 15 and over were on treatment, compared with 74% of men. These differences reflect social and economic barriers, including gender inequality, violence, and limited access to services, which affect testing and treatment uptake.

Geographic disparities are equally pronounced. More than half of all people living with HIV live in eastern and southern Africa, and sub-Saharan Africa accounted for about half of new infections in 2024, the most recent year for which regional breakdowns were published in the same report. Some other regions have seen increases in recent years, such as the Middle East and North Africa, Latin America, and eastern Europe and central Asia, so global averages can obscure distinct regional trajectories. Estimates across all regions should therefore be read alongside their uncertainty ranges and the differing reporting dates of each data source.

Regional and population patterns

Sub-Saharan Africa carries the largest share of the epidemic. In 2025, sub-Saharan Africa accounted for approximately 64 per cent of people of all ages living with HIV and 87 per cent of children and adolescents living with HIV worldwide. Within the region, 21.1 million people living with HIV lived in eastern and southern Africa out of a global total of about 40.9 million. The burden also falls unevenly by sex and age. In eastern and southern Africa, young women aged 15 to 24 make up more than three-quarters of new infections in that age group, and adolescent girls and young women account for 28% of new infections among all age groups. In sub-Saharan Africa, women and girls (all ages) accounted for 63% of all new HIV infections.

Outside sub-Saharan Africa, the pattern is shaped mainly by key populations. UNAIDS defines key populations to include gay men and other men who have sex with men, sex workers, transgender people and people who inject drugs, and WHO also includes people in prisons. Prevalence among these groups is far above the general adult level. Global prevalence is 7.6% among gay men and other men who have sex with men, 2.7% among sex workers, 7.1% among people who inject drugs, 8.5% among transgender people, and 1.4% among people in prisons. Globally, the risk of acquiring HIV is 26 times higher among MSM compared to the general population. Because these groups are small, they can have high prevalence while the overall prevalence in a country remains low. Their share of infections is also growing. In 2022, more than half (55%) of all new HIV infections occurred among people from key populations and their sexual partners, up from an estimated 44% in 2010. New HIV infections declined by 35% between 2010 and 2022 in the 15–49-year-old population globally, but only by 11% among key populations. UNAIDS attributes this gap to discrimination, stigma and criminalization that are preventing access to and/or availability of services for key populations.

Eastern Europe and central Asia is one of the few regions where the epidemic is still expanding. The annual number of new HIV infections in eastern Europe and central Asia continues to rise, reaching 130 000 [110 000–140 000] in 2024—a 7% increase from the 120 000 [100 000–130 000] HIV infections in 2010. Only half of people living with HIV (51% [41–57%]) are receiving treatment, and the region is the only one in which AIDS-related deaths are still increasing, having risen by 48% since 2010. The regional epidemic began largely among people who inject drugs, and an increasing proportion of new HIV infections are as a result of sexual transmission from people who inject drugs or sex work. Infections among gay men and other men who have sex with men have also risen sharply, and in 2022 the number of gay men and other men who have sex with men who acquired HIV was 144% higher than in 2010. The legal environment adds to these risks, since 13 countries specifically criminalize nondisclosure, exposure or transmission of HIV.

Other regions follow different trajectories. Between 2010 and 2024, the number of new HIV infections decreased by 21% in the Caribbean and 17% in Asia and the Pacific, but they increased by 94% in the Middle East and North Africa and 13% in Latin America. In the Middle East and North Africa, the region has about 240,000 people living with HIV, and People living with HIV on ART: 53%, which is lower than in most other regions. In Asia and the Pacific, where MSM accounted for 44% of new HIV infections in Asia and the Pacific (2019 data, UNAIDS).

Epidemiologists distinguish between generalized epidemics, in which HIV spreads widely through the general adult population as in much of southern Africa, and concentrated epidemics, in which prevalence is high within specific networks but stays low in the general population. The distinction determines whether prevention and treatment programmes are targeted broadly or focused on particular groups.

Global response, funding, and access to medicines

The international response is coordinated mainly through the United Nations system. The Joint United Nations Programme on HIV/AIDS (UNAIDS) was created by a 1994 resolution of the UN Economic and Social Council and began operating in January 1996. It brings together the work of several UN agencies and the World Bank, and its role is to advocate for action, mobilize resources, and support national programmes. The World Health Organization complements this by setting clinical guidelines and monitoring progress on the epidemic. The two bodies do different jobs: UNAIDS leads on coordination and strategy, while WHO sets the medical standards that national programmes follow.

Funding for prevention and treatment

Most of the money that supports HIV services in low- and middle-income countries comes from outside those countries. UNAIDS estimated that about $18.7 billion was available for HIV in these countries in 2024, and donor governments supplied roughly 44% of it. The United States has been the largest single international donor. Its President's Emergency Plan for AIDS Relief (PEPFAR), launched in 2003, has directed more than $130 billion toward prevention, care and treatment, and the US is also the largest contributor to the Global Fund to Fight AIDS, Tuberculosis and Malaria. Because of this concentration, decisions about a single donor can affect service delivery across many countries at once.

The 2025 funding disruption

In January 2025 the US government paused foreign aid, closed the US Agency for International Development, and froze PEPFAR-related activity for 90 days. Congress had appropriated $6 billion for PEPFAR for fiscal year 2025, but the Office of Management and Budget released only about $2.9 billion, and that money was listed as unallocated and tied to spending plans. Thousands of implementing partners faced delayed, terminated or altered awards. A survey presented at AIDS 2026 in Rio de Janeiro found that 72% of organisations providing services to key populations had been forced to close those services, and that local providers were hit harder than international NGOs. Modelling by the Burnet Institute, using UNAIDS tools for 26 countries, projected between 4.4 and 10.8 million additional new infections in 2025–2030 if PEPFAR were discontinued, depending on how well mitigation measures worked. Official figures have shown a more mixed picture: the number of people receiving antiretroviral therapy in July–September 2025 was 20.3 million, close to the 20.4 million of a year earlier, while other indicators declined. Researchers and advocacy groups have argued that prevention, community-based services and services for key populations have been the most affected, and some government officials have disputed how large the damage is.

Generic competition and drug prices

The price of antiretroviral drugs has fallen sharply, mainly because of competition among generic manufacturers. The Medécins Sans Frontières Access Campaign has reported that the price of antiretrovirals dropped by more than 99% over roughly a decade, and that a recommended first-line regimen had fallen to around $140 per patient per year by the mid-2010s. Differential pricing, in which originator companies offer lower prices to poorer countries, also played a role. A 2009 analysis found that originator tiered prices in low- and middle-income countries were 23–498% higher than the prices of generic equivalents. Voluntary pooled procurement has produced further savings: a study of generic efavirenz found that prices fell by 16–19% between 2009 and 2013 under this arrangement. The Medicines Patent Pool, established in 2010, negotiates voluntary licences with patent holders so that generic versions can be produced for low- and middle-income countries.

Patents, intellectual property and policy debate

Access problems persist for newer drugs. Patents on these medicines can delay generic entry and prevent the price reductions that come from economies of scale, and the demand for newer, more expensive drugs is growing as people develop resistance or need fewer side effects. Governments can use the flexibilities in the TRIPS Agreement, including compulsory licensing, to address this. Supporters of strong patent protection argue that it sustains pharmaceutical research and development, while critics argue that it limits access in the countries with the highest burden. The debate over how to balance these interests remains active, and it is closely tied to the funding questions above, since lower prices and sustained donor support both determine how many people can be reached.

Stigma, rights, and law

Stigma and discrimination are among the most persistent obstacles in the HIV response, because fear of exposure, rejection, or mistreatment can stop people from being tested, starting treatment, or telling partners and relatives about their status. A pooled analysis of population-based surveys from sub-Saharan Africa found that people living in communities with high levels of discriminatory attitudes toward people with HIV were less likely to have tested, and people with HIV in those communities were less likely to be taking antiretroviral therapy or to reach viral suppression (Where the prevalence of community-level discriminatory attitudes was equal to or above the median, people were less likely to have tested for HIV). Within health services, UNAIDS documents a wide range of abuses, from testing carried out without consent to unauthorized disclosure of a patient's status to family members or employers (HIV-related discrimination can also take many forms, including mandatory HIV testing without consent or appropriate counselling). A UNAIDS fact sheet reports that about one in eight people living with HIV faced stigma or discrimination while seeking HIV-related care in the previous year (13% of people living with HIV experienced stigma and discrimination when seeking HIV-related care in the past 12 months).

Criminal law is one of the most contested areas. Some countries apply HIV-specific statutes that penalize non-disclosure, exposure, or transmission, while others rely on general offences such as assault. The first HIV-specific criminal law was introduced in the United States in 1987 (The USA was the first country to introduce HIV-specific criminal laws in 1987.). Legislative trends differ: Zimbabwe repealed its HIV-specific provisions in 2022 (Zimbabwe in 2022.), Sweden removed the legal duty to disclose HIV status in 2020, while Poland raised the maximum prison term for HIV exposure from three to eight years in the same year (Poland is going in the opposite direction: under the guise of COVID-19 prevention, the country changed its HIV-specific penal provisions in 2020 and increased the prison sentence for HIV exposure from a maximum of three to eight years.). Critics point out that many such laws are broad enough to cover acts carrying little or no risk, such as cases where condom use or low viral load was not recognized (Many allow prosecution for acts that constitute no or very little risk by failing to recognize condom use or low viral load). A 2008 UNAIDS/UNDP policy brief therefore urged countries to limit criminal liability to intentional transmission, meaning cases where a person knows their status, intends to transmit, and actually transmits the virus (First, it urges countries to "limit criminalization to cases of intentional transmission, i.e. where a person knows his or her HIV-positive status, acts with the intention to transmit HIV, and does in fact transmit it").

Published counts of countries with such laws are not directly comparable. A 2019 UNAIDS-based tally reported 92 countries with HIV-specific criminal laws or prosecutions under general law (As of 2019, UNAIDS reports that 92 countries have either HIV‐specific criminal laws and/or have prosecuted individuals under general laws), whereas a 2024 UNAIDS fact sheet states that fewer than 10% of countries have laws criminalizing HIV nondisclosure, exposure, or transmission (Less than 10% of countries have laws criminalizing HIV nondisclosure, exposure or transmission). The gap largely reflects differences in how countries are defined and counted, and the sources do not fully resolve it.

International human rights standards form the main normative framework. UN human rights bodies and experts have concluded that criminalization violates rights to health, privacy, equality, and non-discrimination, and that it impedes treatment and prevention (International human rights bodies and experts have held that HIV criminalization violates human rights, including to health, privacy, equality and non-discrimination, and impedes HIV treatment and prevention). The UN Commission on Human Rights has also interpreted "other status" in non-discrimination clauses to include health status, including HIV/AIDS (The Commission on Human Rights has confirmed that "other status" in non-discrimination provisions in international human rights treaties is to be interpreted to include health status, including HIV/AIDS.). Privacy protections require that people give informed consent to testing and that their HIV-related information remains confidential (This right encompasses obligations to respect physical privacy, including the obligation to seek informed consent to HIV testing, and to respect confidentiality of all information relating to a person's HIV status.). Several national courts have also struck down such laws; in one example, a high court in Saint Lucia decriminalized consensual same-sex relations in 2025, a change UNAIDS welcomed as removing an obstacle to HIV services for gay and other men who have sex with men and for transgender women.

Vulnerability is shaped by gender, legal and economic status, and access to health care. Women prosecuted or merely accused in HIV-related cases can lose housing, custody of their children, access to services, and standing in their communities (Women who are prosecuted or even just accused in HIV-specific cases may lose their homes, custody of their children, access to services, standing in their community, and so much more.). Some national courts have found criminal provisions unconstitutional partly because they discriminate against women (National apex courts and parliaments have found such laws to be unconstitutional, breaching the rights of equality and non-discrimination, including discrimination against women.). Restrictions on movement also affect people with HIV: experts note that the most repressive regulations in parts of the Middle East, North Africa, and Eastern Europe have involved testing without consent, detention before deportation, and denial of treatment (Countries in the Middle East, north Africa, and eastern Europe tend to have the most repressive restrictions with documented cases of people subjected to testing without consent, jailed before deportation, and denied access to HIV treatment.). Where poverty, poor legal aid, and limited health coverage coincide with these risks, people are least able to contest abuses or to keep up with treatment.

Special populations and comorbidities

Most HIV infections in children arise from mother-to-child transmission, which can occur during pregnancy, during delivery, or through breastfeeding. Where safe and affordable infant formula is unavailable, breastfeeding is a major route. Antiretroviral therapy given to the mother can lower the risk of transmission from about 25% to under 1%, so public health programmes focus on testing mothers early and keeping their viral load suppressed. Diagnosing infants differs from diagnosing adults. Maternal antibodies can persist for many months, so children under 18 months are usually tested with nucleic acid assays that detect viral RNA or DNA. Treatment also requires age-appropriate formulations, because adult tablets are often too large or unpalatable and doses must keep pace with rapid growth. Dolutegravir, a well-tolerated and highly effective drug, has expanded pediatric options, but a 2025 study was still needed to establish a suitable dose for newborns at risk. A systematic review of 72 studies found that roughly a third of children had pretreatment drug resistance, with higher rates among infants whose prophylaxis had failed. Adherence support for caregivers is therefore a central part of pediatric care.

Pregnancy calls for treatment that protects both the mother and the infant. The "Option B+" approach, which started all pregnant and breastfeeding women on antiretroviral therapy regardless of CD4 count, helped establish the WHO "treat all" guidance. Drug selection in pregnancy weighs efficacy against the available safety data for the fetus, and some regimens are preferred or avoided for this reason. Sustained suppression of the mother's viral load before delivery is the key requirement for preventing transmission. Infants exposed in utero or during birth usually receive a short course of antiretroviral prophylaxis, and this approach has made the virtual elimination of pediatric infection a realistic long-term goal in settings with good services.

As antiretroviral therapy has extended survival, the population of people with HIV has aged considerably. About 70% of people with HIV in the United States are now 50 or older. Older people with HIV face a heavier burden of non-AIDS conditions, including cardiovascular disease, diabetes, chronic kidney disease, osteoporosis, liver disease, certain cancers, and neurocognitive impairment. Persistent immune activation and inflammation despite viral suppression are thought to contribute to cardiovascular and renal disease, and people with HIV show higher levels of proinflammatory cytokines such as IL-6 even when the virus is controlled. Some older antiretroviral regimens also caused metabolic problems, including dyslipidemia and insulin resistance, although these toxicities have declined with newer drugs. Shared risk factors such as smoking, physical inactivity, and poor diet add to the burden. Analyses of insured adults suggest that people with HIV spend around 15 years more of life with one or more major comorbidities than people without HIV, and that the gap narrows to about 10 years among those who start treatment at a CD4 count above 500. In the United States, heart disease and cancer are the leading causes of death among older people with HIV, and the health-care costs of age-related conditions are substantial.

Coinfections markedly increase illness and death. Tuberculosis remains the leading cause of death among people with HIV. In 2023, about 24% of people with both HIV and TB died, compared with about 11% of people with TB who did not have HIV. WHO estimates that annual HIV-associated TB deaths fell by about 78%, from 740,000 in 2006 to 160,000 in 2023, largely through earlier diagnosis and better treatment. Severe disease is common, and bloodstream infection is found in a substantial share of hospitalized patients with HIV and TB. Chronic hepatitis B and hepatitis C are also important. In a cohort of more than 25,000 people with HIV, hepatitis B coinfection was associated with a higher risk of death from any cause, and the liver-related mortality risk was roughly tenfold higher. Hepatitis C coinfection was similarly linked to elevated liver-related mortality. Human papillomavirus infection, which is associated with anal and cervical cancers, is another concern in this group. Managing these conditions effectively requires integrated care that combines HIV treatment with screening and treatment for the coinfecting illnesses.

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