HIV/AIDS

"AIDS" redirects here. For other uses, see AIDS (disambiguation).

HIV/AIDS
Synonyms	HIV disease, HIV infection [1] [2]
The red ribbon is a symbol for solidarity with HIV-positive people and those living with AIDS. [3]
Specialty	Infectious disease
Symptoms	Early: flu like illness [4] Later: Large lymph nodes, fever, weight loss [4]
Complications	Opportunistic infections, tumors [4]
Duration	Lifelong [4]
Causes	Human immunodeficiency virus (HIV) [4]
Risk factors	Exposure to blood, breast milk, sex [4]
Diagnostic method	Blood tests [4]
Prevention	Safe sex, needle exchange, male circumcision, pre-exposure prophylaxis, post-exposure prophylaxis [4]
Treatment	Antiretroviral therapy [4]
Prognosis	Near normal life expectancy with treatment [5] [6] 11 years life expectancy without treatment [7]
Frequency	1.8 million new cases (2016) [8] 36.7 million living with HIV (2016) [8]
Deaths	1.0 million (2016) [8]

Human immunodeficiency virus infection and acquired immune deficiency syndrome (HIV/AIDS) is a spectrum of conditions caused by infection with the human immunodeficiency virus (HIV). ^{[9] [10] [11]} Following initial infection, a person may not notice any symptoms or may experience a brief period of influenza-like illness. ^[4] Typically, this is followed by a prolonged period with no symptoms. ^[5] As the infection progresses, it interferes more with the immune system, increasing the risk of developing common infections such as tuberculosis, as well as other opportunistic infections, and tumors that rarely affect people who have uncompromised immune systems. ^[4] These late symptoms of infection are referred to as acquired immunodeficiency syndrome (AIDS). ^[5] This stage is often also associated with unintended weight loss. ^[5]

HIV is spread primarily by unprotected sex (including anal and oral sex), contaminated blood transfusions, hypodermic needles, and from mother to child during pregnancy, delivery, or breastfeeding. ^[12] Some bodily fluids, such as saliva and tears, do not transmit HIV. ^[13] Methods of prevention include safe sex, needle exchange programs, treating those who are infected, pre- and post-exposure prophylaxis, and male circumcision. ^[4] Disease in a baby can often be prevented by giving both the mother and child antiretroviral medication. ^[4] There is no cure or vaccine; however, antiretroviral treatment can slow the course of the disease and may lead to a near-normal life expectancy. ^{[5] [6]} Treatment is recommended as soon as the diagnosis is made. ^[14] Without treatment, the average survival time after infection is 11 years. ^[7]

In 2016, about 36.7 million people were living with HIV and it resulted in 1 million deaths. ^[15] There were 300,000 fewer new HIV cases in 2016 than in 2015. ^[16] Most of those infected live in sub-Saharan Africa. ^[4] From the time AIDS was identified in the early 1980s to 2017, the disease has caused an estimated 35 million deaths worldwide. ^[17] HIV/AIDS is considered a pandemic—a disease outbreak which is present over a large area and is actively spreading. ^[18] HIV originated in west-central Africa during the late 19th or early 20th century. ^[19] AIDS was first recognized by the United States Centers for Disease Control and Prevention (CDC) in 1981 and its cause—HIV infection—was identified in the early part of the decade. ^[20]

HIV/AIDS has had a large impact on society, both as an illness and as a source of discrimination. ^[21] The disease also has large economic impacts. ^[21] There are many misconceptions about HIV/AIDS such as the belief that it can be transmitted by casual non-sexual contact. ^[22] The disease has become subject to many controversies involving religion including the Catholic Church's position not to support condom use as prevention. ^[23] It has attracted international medical and political attention as well as large-scale funding since it was identified in the 1980s. ^[24]

Signs and symptoms

Main article: Signs and symptoms of HIV/AIDS

There are three main stages of HIV infection: acute infection, clinical latency, and AIDS. ^{[1] [25]}

Acute infection

Main symptoms of acute HIV infection

The initial period following the contraction of HIV is called acute HIV, primary HIV or acute retroviral syndrome. ^{[25] [26]} Many individuals develop an influenza-like illness or a mononucleosis-like illness 2–4 weeks after exposure while others have no significant symptoms. ^{[27] [28]} Symptoms occur in 40–90% of cases and most commonly include fever, large tender lymph nodes, throat inflammation, a rash, headache, tiredness, and/or sores of the mouth and genitals. ^{[26] [28]} The rash, which occurs in 20–50% of cases, presents itself on the trunk and is maculopapular, classically. ^[29] Some people also develop opportunistic infections at this stage. ^[26] Gastrointestinal symptoms, such as vomiting or diarrhea may occur. ^[28] Neurological symptoms of peripheral neuropathy or Guillain–Barré syndrome also occurs. ^[28] The duration of the symptoms varies, but is usually one or two weeks. ^[28]

Due to their nonspecific character, these symptoms are not often recognized as signs of HIV infection. Even cases that do get seen by a family doctor or a hospital are often misdiagnosed as one of the many common infectious diseases with overlapping symptoms. Thus, it is recommended that HIV be considered in people presenting with an unexplained fever who may have risk factors for the infection. ^[28]

Clinical latency

The initial symptoms are followed by a stage called clinical latency, asymptomatic HIV, or chronic HIV. ^[1] Without treatment, this second stage of the natural history of HIV infection can last from about three years ^[30] to over 20 years ^[31] (on average, about eight years). ^[32] While typically there are few or no symptoms at first, near the end of this stage many people experience fever, weight loss, gastrointestinal problems and muscle pains. ^[1] Between 50 and 70% of people also develop persistent generalized lymphadenopathy, characterized by unexplained, non-painful enlargement of more than one group of lymph nodes (other than in the groin) for over three to six months. ^[25]

Although most HIV-1 infected individuals have a detectable viral load and in the absence of treatment will eventually progress to AIDS, a small proportion (about 5%) retain high levels of CD4⁺ T cells (T helper cells) without antiretroviral therapy for more than 5 years. ^{[28] [33]} These individuals are classified as "HIV controllers" or long-term nonprogressors (LTNP). ^[33] Another group consists of those who maintain a low or undetectable viral load without anti-retroviral treatment, known as "elite controllers" or "elite suppressors". They represent approximately 1 in 300 infected persons. ^[34]

Acquired immunodeficiency syndrome

Main symptoms of AIDS.

Acquired immunodeficiency syndrome (AIDS) is defined in terms of either a CD4⁺ T cell count below 200 cells per µL or the occurrence of specific diseases in association with an HIV infection. ^[28] In the absence of specific treatment, around half of people infected with HIV develop AIDS within ten years. ^[28] The most common initial conditions that alert to the presence of AIDS are pneumocystis pneumonia (40%), cachexia in the form of HIV wasting syndrome (20%), and esophageal candidiasis. ^[28] Other common signs include recurrent respiratory tract infections. ^[28]

Opportunistic infections may be caused by bacteria, viruses, fungi, and parasites that are normally controlled by the immune system. ^[35] Which infections occur depends partly on what organisms are common in the person's environment. ^[28] These infections may affect nearly every organ system. ^[36]

People with AIDS have an increased risk of developing various viral-induced cancers, including Kaposi's sarcoma, Burkitt's lymphoma, primary central nervous system lymphoma, and cervical cancer. ^[29] Kaposi's sarcoma is the most common cancer occurring in 10 to 20% of people with HIV. ^[37] The second most common cancer is lymphoma, which is the cause of death of nearly 16% of people with AIDS and is the initial sign of AIDS in 3 to 4%. ^[37] Both these cancers are associated with human herpesvirus 8 (HHV-8). ^[37] Cervical cancer occurs more frequently in those with AIDS because of its association with human papillomavirus (HPV). ^[37] Conjunctival cancer (of the layer that lines the inner part of eyelids and the white part of the eye) is also more common in those with HIV. ^[38]

Additionally, people with AIDS frequently have systemic symptoms such as prolonged fevers, sweats (particularly at night), swollen lymph nodes, chills, weakness, and unintended weight loss. ^[39] Diarrhea is another common symptom, present in about 90% of people with AIDS. ^[40] They can also be affected by diverse psychiatric and neurological symptoms independent of opportunistic infections and cancers. ^[41]

Transmission

Average per act risk of getting HIV
by exposure route to an infected source

Exposure route	Chance of infection
Blood transfusion	90% [42] [ not in citation given ]
Childbirth (to child)	25% [43] [ clarification needed ]
Needle-sharing injection drug use	0.67% [42]
Percutaneous needle stick	0.30% [44]
Receptive anal intercourse*	0.04–3.0% [45]
Insertive anal intercourse*	0.03% [46]
Receptive penile-vaginal intercourse*	0.05–0.30% [45] [47]
Insertive penile-vaginal intercourse*	0.01–0.38% [45] [47]
Receptive oral intercourse*§	0–0.04% [45]
Insertive oral intercourse*§	0–0.005% [48]
* assuming no condom use § source refers to oral intercourse performed on a man

HIV is spread by three main routes: sexual contact, significant exposure to infected body fluids or tissues, and from mother to child during pregnancy, delivery, or breastfeeding (known as vertical transmission). ^[12] There is no risk of acquiring HIV if exposed to feces, nasal secretions, saliva, sputum, sweat, tears, urine, or vomit unless these are contaminated with blood. ^[49] It is also possible to be co-infected by more than one strain of HIV—a condition known as HIV superinfection. ^[50]

Sexual

The most frequent mode of transmission of HIV is through sexual contact with an infected person. ^[12] However, an HIV-positive person who has an undetectable viral load as a result of long-term treatment has effectively no risk of transmitting HIV sexually. ^{[51] [52]} Globally, the most common mode of HIV transmission is via sexual contacts between people of the opposite sex; ^[12] however, the pattern of transmission varies among countries. As of 2014 ^[update] , most HIV transmission in the United States occurred among men who had sex with men (83% of new HIV diagnoses among males aged 13 and older and 67% of total new diagnoses). ^[53] In the US, gay and bisexual men aged 13 to 24 accounted for an estimated 92% of new HIV diagnoses among all men in their age group and 27% of new diagnoses among all gay and bisexual men. ^[53] About 15% of gay and bisexual men have HIV while 28% of transgender women test positive in the US. ^{[53] [54]}

With regard to unprotected heterosexual contacts, estimates of the risk of HIV transmission per sexual act appear to be four to ten times higher in low-income countries than in high-income countries. ^[55] In low-income countries, the risk of female-to-male transmission is estimated as 0.38% per act, and of male-to-female transmission as 0.30% per act; the equivalent estimates for high-income countries are 0.04% per act for female-to-male transmission, and 0.08% per act for male-to-female transmission. ^[55] The risk of transmission from anal intercourse is especially high, estimated as 1.4–1.7% per act in both heterosexual and homosexual contacts. ^{[55] [56]} While the risk of transmission from oral sex is relatively low, it is still present. ^[57] The risk from receiving oral sex has been described as "nearly nil"; ^[58] however, a few cases have been reported. ^[59] The per-act risk is estimated at 0–0.04% for receptive oral intercourse. ^[60] In settings involving prostitution in low income countries, risk of female-to-male transmission has been estimated as 2.4% per act and male-to-female transmission as 0.05% per act. ^[55]

Risk of transmission increases in the presence of many sexually transmitted infections ^[61] and genital ulcers. ^[55] Genital ulcers appear to increase the risk approximately fivefold. ^[55] Other sexually transmitted infections, such as gonorrhea, chlamydia, trichomoniasis, and bacterial vaginosis, are associated with somewhat smaller increases in risk of transmission. ^[60]

The viral load of an infected person is an important risk factor in both sexual and mother-to-child transmission. ^[62] During the first 2.5 months of an HIV infection a person's infectiousness is twelve times higher due to the high viral load associated with acute HIV. ^[60] If the person is in the late stages of infection, rates of transmission are approximately eightfold greater. ^[55]

Commercial sex workers (including those in pornography) have an increased likelihood of contracting HIV. ^{[63] [64]} Rough sex can be a factor associated with an increased risk of transmission. ^[65] Sexual assault is also believed to carry an increased risk of HIV transmission as condoms are rarely worn, physical trauma to the vagina or rectum is likely, and there may be a greater risk of concurrent sexually transmitted infections. ^[66]

Body fluids

CDC poster from 1989 highlighting the threat of AIDS associated with drug use

The second most frequent mode of HIV transmission is via blood and blood products. ^[12] Blood-borne transmission can be through needle-sharing during intravenous drug use, needle stick injury, transfusion of contaminated blood or blood product, or medical injections with unsterilized equipment. The risk from sharing a needle during drug injection is between 0.63 and 2.4% per act, with an average of 0.8%. ^[67] The risk of acquiring HIV from a needle stick from an HIV-infected person is estimated as 0.3% (about 1 in 333) per act and the risk following mucous membrane exposure to infected blood as 0.09% (about 1 in 1000) per act. ^[49] In the United States intravenous drug users made up 12% of all new cases of HIV in 2009, ^[68] and in some areas more than 80% of people who inject drugs are HIV positive. ^[12]

HIV is transmitted in about 93% of blood transfusions using infected blood. ^[67] In developed countries the risk of acquiring HIV from a blood transfusion is extremely low (less than one in half a million) where improved donor selection and HIV screening is performed; ^[12] for example, in the UK the risk is reported at one in five million ^[69] and in the United States it was one in 1.5 million in 2008. ^[70] In low income countries, only half of transfusions may be appropriately screened (as of 2008), ^[71] and it is estimated that up to 15% of HIV infections in these areas come from transfusion of infected blood and blood products, representing between 5% and 10% of global infections. ^{[12] [72]} Although rare because of screening, it is possible to acquire HIV from organ and tissue transplantation. ^[73]

Unsafe medical injections play a significant role in HIV spread in sub-Saharan Africa. In 2007, between 12 and 17% of infections in this region were attributed to medical syringe use. ^[74] The World Health Organization estimates the risk of transmission as a result of a medical injection in Africa at 1.2%. ^[74] Significant risks are also associated with invasive procedures, assisted delivery, and dental care in this area of the world. ^[74]

People giving or receiving tattoos, piercings, and scarification are theoretically at risk of infection but no confirmed cases have been documented. ^[75] It is not possible for mosquitoes or other insects to transmit HIV. ^[76]

Mother-to-child

Main articles: HIV and pregnancy and HIV and breastfeeding

HIV can be transmitted from mother to child during pregnancy, during delivery, or through breast milk, resulting in the baby also contracting HIV. ^{[77] [78]} This is the third most common way in which HIV is transmitted globally. ^[12] In the absence of treatment, the risk of transmission before or during birth is around 20% and in those who also breastfeed 35%. ^[78] As of 2008, vertical transmission accounted for about 90% of cases of HIV in children. ^[78] With appropriate treatment the risk of mother-to-child infection can be reduced to about 1%. ^[78] Preventive treatment involves the mother taking antiretrovirals during pregnancy and delivery, an elective caesarean section, avoiding breastfeeding, and administering antiretroviral drugs to the newborn. ^[79] Antiretrovirals when taken by either the mother or the infant decrease the risk of transmission in those who do breastfeed. ^[80] However, many of these measures are not available in the developing world. ^[79] If blood contaminates food during pre-chewing it may pose a risk of transmission. ^[75]

If a woman is untreated, two years of breastfeeding results in an HIV/AIDS risk in her baby of about 17%. Treatment decreases this risk to 1 to 2% per year. Due to the increased risk of death without breastfeeding in many areas in the developing world, the World Health Organization recommends either: (1) the mother and baby being treated with antiretroviral medication while breastfeeding being continued (2) the provision of safe formula. ^[81] Infection with HIV during pregnancy is also associated with miscarriage. ^[82]

Virology

Main article: HIV

Diagram of a HIV virion structure

Scanning electron micrograph of HIV-1, colored green, budding from a cultured lymphocyte.

HIV is the cause of the spectrum of disease known as HIV/AIDS. HIV is a retrovirus that primarily infects components of the human immune system such as CD4⁺ T cells, macrophages and dendritic cells. It directly and indirectly destroys CD4⁺ T cells. ^[83]

HIV is a member of the genus Lentivirus , ^[84] part of the family Retroviridae . ^[85] Lentiviruses share many morphological and biological characteristics. Many species of mammals are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. ^[86] Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry into the target cell, the viral RNA genome is converted (reverse transcribed) into double-stranded DNA by a virally encoded reverse transcriptase that is transported along with the viral genome in the virus particle. The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded integrase and host co-factors. ^[87] Once integrated, the virus may become latent, allowing the virus and its host cell to avoid detection by the immune system. ^[88] Alternatively, the virus may be transcribed, producing new RNA genomes and viral proteins that are packaged and released from the cell as new virus particles that begin the replication cycle anew. ^[89]

HIV is now known to spread between CD4⁺ T cells by two parallel routes: cell-free spread and cell-to-cell spread, i.e. it employs hybrid spreading mechanisms. ^[90] In the cell-free spread, virus particles bud from an infected T cell, enter the blood/extracellular fluid and then infect another T cell following a chance encounter. ^[90] HIV can also disseminate by direct transmission from one cell to another by a process of cell-to-cell spread. ^{[91] [92]} The hybrid spreading mechanisms of HIV contribute to the virus's ongoing replication against antiretroviral therapies. ^{[90] [93]}

Two types of HIV have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was originally discovered (and initially referred to also as LAV or HTLV-III). It is more virulent, more infective, ^[94] and is the cause of the majority of HIV infections globally. The lower infectivity of HIV-2 as compared with HIV-1 implies that fewer people exposed to HIV-2 will be infected per exposure. Because of its relatively poor capacity for transmission, HIV-2 is largely confined to West Africa. ^[95]

Pathophysiology

Main article: Pathophysiology of HIV/AIDS

HIV/AIDS explained in a simple way

HIV replication cycle

After the virus enters the body there is a period of rapid viral replication, leading to an abundance of virus in the peripheral blood. During primary infection, the level of HIV may reach several million virus particles per milliliter of blood. ^[96] This response is accompanied by a marked drop in the number of circulating CD4⁺ T cells. The acute viremia is almost invariably associated with activation of CD8⁺ T cells, which kill HIV-infected cells, and subsequently with antibody production, or seroconversion. The CD8⁺ T cell response is thought to be important in controlling virus levels, which peak and then decline, as the CD4⁺ T cell counts recover. A good CD8⁺ T cell response has been linked to slower disease progression and a better prognosis, though it does not eliminate the virus. ^[97]

Ultimately, HIV causes AIDS by depleting CD4⁺ T cells. This weakens the immune system and allows opportunistic infections. T cells are essential to the immune response and without them, the body cannot fight infections or kill cancerous cells. The mechanism of CD4⁺ T cell depletion differs in the acute and chronic phases. ^[98] During the acute phase, HIV-induced cell lysis and killing of infected cells by cytotoxic T cells accounts for CD4⁺ T cell depletion, although apoptosis may also be a factor. During the chronic phase, the consequences of generalized immune activation coupled with the gradual loss of the ability of the immune system to generate new T cells appear to account for the slow decline in CD4⁺ T cell numbers. ^[99]

Although the symptoms of immune deficiency characteristic of AIDS do not appear for years after a person is infected, the bulk of CD4⁺ T cell loss occurs during the first weeks of infection, especially in the intestinal mucosa, which harbors the majority of the lymphocytes found in the body. ^[100] The reason for the preferential loss of mucosal CD4⁺ T cells is that the majority of mucosal CD4⁺ T cells express the CCR5 protein which HIV uses as a co-receptor to gain access to the cells, whereas only a small fraction of CD4⁺ T cells in the bloodstream do so. ^[101] A specific genetic change that alters the CCR5 protein when present in both chromosomes very effectively prevents HIV-1 infection. ^[102]

HIV seeks out and destroys CCR5 expressing CD4⁺ T cells during acute infection. ^[103] A vigorous immune response eventually controls the infection and initiates the clinically latent phase. CD4⁺ T cells in mucosal tissues remain particularly affected. ^[103] Continuous HIV replication causes a state of generalized immune activation persisting throughout the chronic phase. ^[104] Immune activation, which is reflected by the increased activation state of immune cells and release of pro-inflammatory cytokines, results from the activity of several HIV gene products and the immune response to ongoing HIV replication. It is also linked to the breakdown of the immune surveillance system of the gastrointestinal mucosal barrier caused by the depletion of mucosal CD4⁺ T cells during the acute phase of disease. ^[105]

Diagnosis

Main article: Diagnosis of HIV/AIDS

A generalized graph of the relationship between HIV copies (viral load) and CD4 T cell counts over the average course of untreated HIV infection.

  CD4 T Lymphocyte count (cells/mm³)

  HIV RNA copies per mL of plasma

Days after exposure needed for the test to be accurate ^[106]

Blood test	Days
Antibody test (rapid test, ELISA 3rd gen)	23–90
Antibody and p24 antigen test (ELISA 4th gen)	18–45
PCR	10–33

HIV/AIDS is diagnosed via laboratory testing and then staged based on the presence of certain signs or symptoms. ^[26] HIV screening is recommended by the United States Preventive Services Task Force for all people 15 years to 65 years of age including all pregnant women. ^[107] Additionally, testing is recommended for those at high risk, which includes anyone diagnosed with a sexually transmitted illness. ^[29] In many areas of the world, a third of HIV carriers only discover they are infected at an advanced stage of the disease when AIDS or severe immunodeficiency has become apparent. ^[29]

HIV testing

Most people infected with HIV develop specific antibodies (i.e. seroconvert) within three to twelve weeks after the initial infection. ^[28] Diagnosis of primary HIV before seroconversion is done by measuring HIV-RNA or p24 antigen. ^[28] Positive results obtained by antibody or PCR testing are confirmed either by a different antibody or by PCR. ^[26]

Antibody tests in children younger than 18 months are typically inaccurate due to the continued presence of maternal antibodies. ^[108] Thus HIV infection can only be diagnosed by PCR testing for HIV RNA or DNA, or via testing for the p24 antigen. ^[26] Much of the world lacks access to reliable PCR testing and many places simply wait until either symptoms develop or the child is old enough for accurate antibody testing. ^[108] In sub-Saharan Africa as of 2007–2009, between 30 and 70% of the population were aware of their HIV status. ^[109] In 2009, between 3.6 and 42% of men and women in Sub-Saharan countries were tested ^[109] which represented a significant increase compared to previous years. ^[109]

Classifications

Two main clinical staging systems are used to classify HIV and HIV-related disease for surveillance purposes: the WHO disease staging system for HIV infection and disease, ^[26] and the CDC classification system for HIV infection. ^[110] The CDC's classification system is more frequently adopted in developed countries. Since the WHO's staging system does not require laboratory tests, it is suited to the resource-restricted conditions encountered in developing countries, where it can also be used to help guide clinical management. Despite their differences, the two systems allow comparison for statistical purposes. ^{[25] [26] [110]}

The World Health Organization first proposed a definition for AIDS in 1986. ^[26] Since then, the WHO classification has been updated and expanded several times, with the most recent version being published in 2007. ^[26] The WHO system uses the following categories:

• Primary HIV infection: May be either asymptomatic or associated with acute retroviral syndrome. ^[26]
• Stage I: HIV infection is asymptomatic with a CD4⁺ T cell count (also known as CD4 count) greater than 500 per microlitre (µl or cubic mm) of blood. ^[26] May include generalized lymph node enlargement. ^[26]
• Stage II: Mild symptoms which may include minor mucocutaneous manifestations and recurrent upper respiratory tract infections. A CD4 count of less than 500/µl. ^[26]
• Stage III: Advanced symptoms which may include unexplained chronic diarrhea for longer than a month, severe bacterial infections including tuberculosis of the lung, and a CD4 count of less than 350/µl. ^[26]
• Stage IV or AIDS: severe symptoms which include toxoplasmosis of the brain, candidiasis of the esophagus, trachea, bronchi or lungs and Kaposi's sarcoma. A CD4 count of less than 200/µl. ^[26]

The United States Center for Disease Control and Prevention also created a classification system for HIV, and updated it in 2008 and 2014. ^{[110] [111]} This system classifies HIV infections based on CD4 count and clinical symptoms, and describes the infection in five groups. ^[111] In those greater than six years of age it is: ^[111]

• Stage 0: the time between a negative or indeterminate HIV test followed less than 180 days by a positive test.
• Stage 1: CD4 count ≥ 500 cells/µl and no AIDS defining conditions.
• Stage 2: CD4 count 200 to 500 cells/µl and no AIDS defining conditions.
• Stage 3: CD4 count ≤ 200 cells/µl or AIDS defining conditions.
• Unknown: if insufficient information is available to make any of the above classifications.

For surveillance purposes, the AIDS diagnosis still stands even if, after treatment, the CD4⁺ T cell count rises to above 200 per µL of blood or other AIDS-defining illnesses are cured. ^[25]

Prevention

Main article: Prevention of HIV/AIDS

AIDS Clinic, McLeod Ganj, Himachal Pradesh, India, 2010

Sexual contact

Consistent condom use reduces the risk of HIV transmission by approximately 80% over the long term. ^[112] When condoms are used consistently by a couple in which one person is infected, the rate of HIV infection is less than 1% per year. ^[113] There is some evidence to suggest that female condoms may provide an equivalent level of protection. ^[114] Application of a vaginal gel containing tenofovir (a reverse transcriptase inhibitor) immediately before sex seems to reduce infection rates by approximately 40% among African women. ^[115] By contrast, use of the spermicide nonoxynol-9 may increase the risk of transmission due to its tendency to cause vaginal and rectal irritation. ^[116]

Circumcision in Sub-Saharan Africa "reduces the acquisition of HIV by heterosexual men by between 38% and 66% over 24 months". ^[117] Due to these studies, both the World Health Organization and UNAIDS recommended male circumcision in 2007 as a method of preventing female-to-male HIV transmission in areas with high rates of HIV. ^[118] However, whether it protects against male-to-female transmission is disputed, ^{[119] [120]} and whether it is of benefit in developed countries and among men who have sex with men is undetermined. ^{[121] [122] [123]} The International Antiviral Society, however, does recommend it for all sexually active heterosexual males and that it be discussed as an option with men who have sex with men. ^[124] Some experts fear that a lower perception of vulnerability among circumcised men may cause more sexual risk-taking behavior, thus negating its preventive effects. ^[125]

Programs encouraging sexual abstinence do not appear to affect subsequent HIV risk. ^[126] Evidence of any benefit from peer education is equally poor. ^[127] Comprehensive sexual education provided at school may decrease high risk behavior. ^{[128] [129]} A substantial minority of young people continues to engage in high-risk practices despite knowing about HIV/AIDS, underestimating their own risk of becoming infected with HIV. ^[130] Voluntary counseling and testing people for HIV does not affect risky behavior in those who test negative but does increase condom use in those who test positive. ^[131] It is not known whether treating other sexually transmitted infections is effective in preventing HIV. ^[61]

Pre-exposure

Antiretroviral treatment among people with HIV whose CD4 count ≤ 550 cells/µL is a very effective way to prevent HIV infection of their partner (a strategy known as treatment as prevention, or TASP). ^[132] TASP is associated with a 10 to 20 fold reduction in transmission risk. ^{[132] [133]} Pre-exposure prophylaxis (PrEP) with a daily dose of the medications tenofovir, with or without emtricitabine, is effective in a number of groups including men who have sex with men, couples where one is HIV positive, and young heterosexuals in Africa. ^[115] It may also be effective in intravenous drug users with a study finding a decrease in risk of 0.7 to 0.4 per 100 person years. ^[134] The USPSTF, ini a 2018 draft, recommended PrEP in those who are at high risk. ^[135]

Universal precautions within the health care environment are believed to be effective in decreasing the risk of HIV. ^[136] Intravenous drug use is an important risk factor and harm reduction strategies such as needle-exchange programs and opioid substitution therapy appear effective in decreasing this risk. ^{[137] [138]}

Post-exposure

A course of antiretrovirals administered within 48 to 72 hours after exposure to HIV-positive blood or genital secretions is referred to as post-exposure prophylaxis (PEP). ^[139] The use of the single agent zidovudine reduces the risk of a HIV infection five-fold following a needle-stick injury. ^[139] As of 2013 ^[update] , the prevention regimen recommended in the United States consists of three medications—tenofovir, emtricitabine and raltegravir—as this may reduce the risk further. ^[140]

PEP treatment is recommended after a sexual assault when the perpetrator is known to be HIV positive, but is controversial when their HIV status is unknown. ^[141] The duration of treatment is usually four weeks ^[142] and is frequently associated with adverse effects—where zidovudine is used, about 70% of cases result in adverse effects such as nausea (24%), fatigue (22%), emotional distress (13%) and headaches (9%). ^[49]

Mother-to-child

Main article: HIV and pregnancy

Programs to prevent the vertical transmission of HIV (from mothers to children) can reduce rates of transmission by 92–99%. ^{[78] [137]} This primarily involves the use of a combination of antiviral medications during pregnancy and after birth in the infant and potentially includes bottle feeding rather than breastfeeding. ^{[78] [143]} If replacement feeding is acceptable, feasible, affordable, sustainable, and safe, mothers should avoid breastfeeding their infants; however exclusive breastfeeding is recommended during the first months of life if this is not the case. ^[144] If exclusive breastfeeding is carried out, the provision of extended antiretroviral prophylaxis to the infant decreases the risk of transmission. ^[145] In 2015, Cuba became the first country in the world to eradicate mother-to-child transmission of HIV. ^[146]

Vaccination

Main article: HIV vaccine

Currently, there is no licensed vaccine for HIV or AIDS. ^[6] The most effective vaccine trial to date, RV 144, was published in 2009 and found a partial reduction in the risk of transmission of roughly 30%, stimulating some hope in the research community of developing a truly effective vaccine. ^[147] Further trials of the RV 144 vaccine are ongoing. ^{[148] [149]}

Treatment

Main article: Management of HIV/AIDS

There is currently no cure or effective HIV vaccine. Treatment consists of highly active antiretroviral therapy (HAART) which slows progression of the disease. ^[150] As of 2010 ^[update] more than 6.6 million people were taking them in low and middle income countries. ^[151] Treatment also includes preventive and active treatment of opportunistic infections.

Antiviral therapy

Stribild – a common once-daily ART regime consisting of elvitegravir, emtricitabine, tenofovir and the booster cobicistat

Current HAART options are combinations (or "cocktails") consisting of at least three medications belonging to at least two types, or "classes," of antiretroviral agents. ^[152] Initially treatment is typically a non-nucleoside reverse transcriptase inhibitor (NNRTI) plus two nucleoside analog reverse transcriptase inhibitors (NRTIs). ^[153] Typical NRTIs include: zidovudine (AZT) or tenofovir (TDF) and lamivudine (3TC) or emtricitabine (FTC). ^[153] Combinations of agents which include protease inhibitors (PI) are used if the above regimen loses effectiveness. ^[152]

The World Health Organization and United States recommends antiretrovirals in people of all ages including pregnant women as soon as the diagnosis is made regardless of CD4 count. ^{[14] [124] [154]} Once treatment is begun it is recommended that it is continued without breaks or "holidays". ^[29] Many people are diagnosed only after treatment ideally should have begun. ^[29] The desired outcome of treatment is a long term plasma HIV-RNA count below 50 copies/mL. ^[29] Levels to determine if treatment is effective are initially recommended after four weeks and once levels fall below 50 copies/mL checks every three to six months are typically adequate. ^[29] Inadequate control is deemed to be greater than 400 copies/mL. ^[29] Based on these criteria treatment is effective in more than 95% of people during the first year. ^[29]

Benefits of treatment include a decreased risk of progression to AIDS and a decreased risk of death. ^[155] In the developing world treatment also improves physical and mental health. ^[156] With treatment there is a 70% reduced risk of acquiring tuberculosis. ^[152] Additional benefits include a decreased risk of transmission of the disease to sexual partners and a decrease in mother-to-child transmission. ^{[152] [157]} The effectiveness of treatment depends to a large part on compliance. ^[29] Reasons for non-adherence include poor access to medical care, ^[158] inadequate social supports, mental illness and drug abuse. ^[159] The complexity of treatment regimens (due to pill numbers and dosing frequency) and adverse effects may reduce adherence. ^[160] Even though cost is an important issue with some medications, ^[161] 47% of those who needed them were taking them in low and middle income countries as of 2010 ^{[update] [151]} and the rate of adherence is similar in low-income and high-income countries. ^[162]

Specific adverse events are related to the antiretroviral agent taken. ^[163] Some relatively common adverse events include: lipodystrophy syndrome, dyslipidemia, and diabetes mellitus, especially with protease inhibitors. ^[25] Other common symptoms include diarrhea, ^{[163] [164]} and an increased risk of cardiovascular disease. ^[165] Newer recommended treatments are associated with fewer adverse effects. ^[29] Certain medications may be associated with birth defects and therefore may be unsuitable for women hoping to have children. ^[29]

Treatment recommendations for children are somewhat different from those for adults. The World Health Organization recommends treating all children less than 5 years of age; children above 5 are treated like adults. ^[166] The United States guidelines recommend treating all children less than 12 months of age and all those with HIV RNA counts greater than 100,000 copies/mL between one year and five years of age. ^[167]

Opportunistic infections

Measures to prevent opportunistic infections are effective in many people with HIV/AIDS. In addition to improving current disease, treatment with antiretrovirals reduces the risk of developing additional opportunistic infections. ^[163] Adults and adolescents who are living with HIV (even on anti-retroviral therapy) with no evidence of active tuberculosis in settings with high tuberculosis burden should receive isoniazid preventive therapy (IPT), the tuberculin skin test can be used to help decide if IPT is needed. ^[168] Vaccination against hepatitis A and B is advised for all people at risk of HIV before they become infected; however it may also be given after infection. ^[169] Trimethoprim/sulfamethoxazole prophylaxis between four and six weeks of age and ceasing breastfeeding in infants born to HIV positive mothers is recommended in resource limited settings. ^[170] It is also recommended to prevent PCP when a person's CD4 count is below 200 cells/uL and in those who have or have previously had PCP. ^[171] People with substantial immunosuppression are also advised to receive prophylactic therapy for toxoplasmosis and MAC. ^[172] Appropriate preventive measures have reduced the rate of these infections by 50% between 1992 and 1997. ^[173] Influenza vaccination and pneumococcal polysaccharide vaccine are often recommended in people with HIV/AIDS with some evidence of benefit. ^{[174] [175]}

Diet

Main article: Nutrition and HIV/AIDS

The World Health Organization (WHO) has issued recommendations regarding nutrient requirements in HIV/AIDS. ^[176] A generally healthy diet is promoted. Dietary intake of micronutrients at RDA levels by HIV-infected adults is recommended by the WHO; higher intake of vitamin A, zinc, and iron can produce adverse effects in HIV positive adults, and is not recommended unless there is documented deficiency. ^{[176] [177] [178] [179]} Dietary supplementation for people who are infected with HIV and who have inadequate nutrition or dietary deficiencies may strengthen their immune systems or help them recover from infections, however evidence indicating an overall benefit in morbidity or reduction in mortality is not consistent. ^[180]

Evidence for supplementation with selenium is mixed with some tentative evidence of benefit. ^[181] For pregnant and lactating women with HIV, multivitamin supplement improves outcomes for both mothers and children. ^[182] If the pregnant or lactating mother has been advised to take anti-retroviral medication to prevent mother-to-child HIV transmission, multivitamin supplements should not replace these treatments. ^[182] There is some evidence that vitamin A supplementation in children with an HIV infection reduces mortality and improves growth. ^[183]

Alternative medicine

In the US, approximately 60% of people with HIV use various forms of complementary or alternative medicine, ^[184] even though the effectiveness of most of these therapies has not been established. ^[185] There is not enough evidence to support the use of herbal medicines. ^[186] There is insufficient evidence to recommend or support the use of medical cannabis to try to increase appetite or weight gain. ^[187]

Prognosis

Deaths due to HIV/AIDS per million persons in 2012

  0

  1–4

  5–12

  13–34

  35–61

  62–134

  135–215

  216–458

  459–1,402

  1,403–5,828

HIV/AIDS has become a chronic rather than an acutely fatal disease in many areas of the world. ^[188] Prognosis varies between people, and both the CD4 count and viral load are useful for predicted outcomes. ^[28] Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype. ^[7] After the diagnosis of AIDS, if treatment is not available, survival ranges between 6 and 19 months. ^{[189] [190]} HAART and appropriate prevention of opportunistic infections reduces the death rate by 80%, and raises the life expectancy for a newly diagnosed young adult to 20–50 years. ^{[188] [191] [192]} This is between two thirds ^[191] and nearly that of the general population. ^{[29] [193]} If treatment is started late in the infection, prognosis is not as good: ^[29] for example, if treatment is begun following the diagnosis of AIDS, life expectancy is ~10–40 years. ^{[29] [188]} Half of infants born with HIV die before two years of age without treatment. ^[170]

Disability-adjusted life year for HIV and AIDS per 100,000 inhabitants as of 2004.

no data   ≤ 10   10–25   25–50   50–100

100–500   500–1000   1,000–2,500   2,500–5,000   5,000–7500

7,500–10,000   10,000–50,000   ≥ 50,000

The primary causes of death from HIV/AIDS are opportunistic infections and cancer, both of which are frequently the result of the progressive failure of the immune system. ^{[173] [194]} Risk of cancer appears to increase once the CD4 count is below 500/μL. ^[29] The rate of clinical disease progression varies widely between individuals and has been shown to be affected by a number of factors such as a person's susceptibility and immune function; ^[195] their access to health care, the presence of co-infections; ^{[189] [196]} and the particular strain (or strains) of the virus involved. ^{[197] [198]}

Tuberculosis co-infection is one of the leading causes of sickness and death in those with HIV/AIDS being present in a third of all HIV-infected people and causing 25% of HIV-related deaths. ^[199] HIV is also one of the most important risk factors for tuberculosis. ^[200] Hepatitis C is another very common co-infection where each disease increases the progression of the other. ^[201] The two most common cancers associated with HIV/AIDS are Kaposi's sarcoma and AIDS-related non-Hodgkin's lymphoma. ^[194] Other cancers that are more frequent include anal cancer, Burkitt's lymphoma, primary central nervous system lymphoma, and cervical cancer. ^{[29] [202]}

Even with anti-retroviral treatment, over the long term HIV-infected people may experience neurocognitive disorders, ^[203] osteoporosis, ^[204] neuropathy, ^[205] cancers, ^{[206] [207]} nephropathy, ^[208] and cardiovascular disease. ^[164] Some conditions, such as lipodystrophy, may be caused both by HIV and its treatment. ^[164]

Epidemiology

Main article: Epidemiology of HIV/AIDS

Estimated percentage of HIV among young adults (15–49) per country as of 2011.

No data   <0.10   0.10–0.5   0.5–1

1–5   5–15   15–50

HIV/AIDS is a global pandemic. ^[210] As of 2016 ^[update] , approximately 36.7 million people have HIV worldwide with the number of new infections that year being about 1.8 million. ^[15] This is down from 3.1 million new infections in 2001. ^[211] Slightly over half the infected population are women and 2.1 million are children. ^[15] It resulted in about 1 million deaths in 2016, down from a peak of 1.9 million in 2005. ^[15]

Sub-Saharan Africa is the region most affected. In 2010, an estimated 68% (22.9 million) of all HIV cases and 66% of all deaths (1.2 million) occurred in this region. ^[212] This means that about 5% of the adult population is infected ^[213] and it is believed to be the cause of 10% of all deaths in children. ^[214] Here in contrast to other regions women compose nearly 60% of cases. ^[212] South Africa has the largest population of people with HIV of any country in the world at 5.9 million. ^[212] Life expectancy has fallen in the worst-affected countries due to HIV/AIDS; for example, in 2006 it was estimated that it had dropped from 65 to 35 years in Botswana. ^[18] Mother-to-child transmission, as of 2013 ^[update] , in Botswana and South Africa has decreased to less than 5% with improvement in many other African nations due to improved access to antiretroviral therapy. ^[215]

South & South East Asia is the second most affected; in 2010 this region contained an estimated 4 million cases or 12% of all people living with HIV resulting in approximately 250,000 deaths. ^[213] Approximately 2.4 million of these cases are in India. ^[212]

In 2008 in the United States approximately 1.2 million people were living with HIV, resulting in about 17,500 deaths. The US Centers for Disease Control and Prevention estimated that in 2008 20% of infected Americans were unaware of their infection. ^[216] As of 2016 ^[update] about 675,000 people have died of HIV/AIDS in the US since the beginning of the HIV epidemic. ^[54] In the United Kingdom as of 2015 ^[update] there were approximately 101,200 cases which resulted in 594 deaths. ^[217] In Canada as of 2008 there were about 65,000 cases causing 53 deaths. ^[218] Between the first recognition of AIDS in 1981 and 2009 it has led to nearly 30 million deaths. ^[219] Prevalence is lowest in Middle East and North Africa at 0.1% or less, East Asia at 0.1% and Western and Central Europe at 0.2%. ^[213] The worst affected European countries, in 2009 and 2012 estimates, are Russia, Ukraine, Latvia, Moldova, Portugal and Belarus, in decreasing order of prevalence. ^[220]

History

Main article: History of HIV/AIDS

Discovery

The Morbidity and Mortality Weekly Report reported in 1981 on what was later to be called "AIDS".

AIDS was first clinically reported on June 5th 1981 with 5 cases in the United States. ^{[37] [221]} The initial cases were a cluster of injecting drug users and homosexual men with no known cause of impaired immunity who showed symptoms of Pneumocystis carinii pneumonia (PCP), a rare opportunistic infection that was known to occur in people with very compromised immune systems. ^[222] Soon thereafter, an unexpected number of homosexual men developed a previously rare skin cancer called Kaposi's sarcoma (KS). ^{[223] [224]} Many more cases of PCP and KS emerged, alerting U.S. Centers for Disease Control and Prevention (CDC) and a CDC task force was formed to monitor the outbreak. ^[225]

In the early days, the CDC did not have an official name for the disease, often referring to it by way of the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus. ^{[226] [227]} They also used Kaposi's sarcoma and opportunistic infections, the name by which a task force had been set up in 1981. ^[228] At one point, the CDC coined the phrase "the 4H disease", since the syndrome seemed to affect heroin users, homosexuals, hemophiliacs, and Haitians. ^{[229] [230]} In the general press, the term "GRID", which stood for gay-related immune deficiency, had been coined. ^[231] However, after determining that AIDS was not isolated to the gay community, ^[228] it was realized that the term GRID was misleading and the term AIDS was introduced at a meeting in July 1982. ^[232] By September 1982 the CDC started referring to the disease as AIDS. ^[233]

In 1983, two separate research groups led by Robert Gallo and Luc Montagnier declared that a novel retrovirus may have been infecting people with AIDS, and published their findings in the same issue of the journal Science . ^{[234] [235]} Gallo claimed that a virus his group had isolated from a person with AIDS was strikingly similar in shape to other human T-lymphotropic viruses (HTLVs) his group had been the first to isolate. Gallo's group called their newly isolated virus HTLV-III. At the same time, Montagnier's group isolated a virus from a person presenting with swelling of the lymph nodes of the neck and physical weakness, two characteristic symptoms of AIDS. Contradicting the report from Gallo's group, Montagnier and his colleagues showed that core proteins of this virus were immunologically different from those of HTLV-I. Montagnier's group named their isolated virus lymphadenopathy-associated virus (LAV). ^[225] As these two viruses turned out to be the same, in 1986, LAV and HTLV-III were renamed HIV. ^[236]

Origins

Left to right: the African green monkey source of SIV, the sooty mangabey source of HIV-2 and the chimpanzee source of HIV-1

Both HIV-1 and HIV-2 are believed to have originated in non-human primates in West-central Africa and were transferred to humans in the early 20th century. ^[19] HIV-1 appears to have originated in southern Cameroon through the evolution of SIV(cpz), a simian immunodeficiency virus (SIV) that infects wild chimpanzees (HIV-1 descends from the SIVcpz endemic in the chimpanzee subspecies Pan troglodytes troglodytes). ^{[237] [238]} The closest relative of HIV-2 is SIV(smm), a virus of the sooty mangabey (Cercocebus atys atys), an Old World monkey living in coastal West Africa (from southern Senegal to western Côte d'Ivoire). ^[95] New World monkeys such as the owl monkey are resistant to HIV-1 infection, possibly because of a genomic fusion of two viral resistance genes. ^[239] HIV-1 is thought to have jumped the species barrier on at least three separate occasions, giving rise to the three groups of the virus, M, N, and O. ^[240]

There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV. ^[241] However, SIV is a weak virus which is typically suppressed by the human immune system within weeks of infection. It is thought that several transmissions of the virus from individual to individual in quick succession are necessary to allow it enough time to mutate into HIV. ^[242] Furthermore, due to its relatively low person-to-person transmission rate, SIV can only spread throughout the population in the presence of one or more high-risk transmission channels, which are thought to have been absent in Africa before the 20th century.

Specific proposed high-risk transmission channels, allowing the virus to adapt to humans and spread throughout the society, depend on the proposed timing of the animal-to-human crossing. Genetic studies of the virus suggest that the most recent common ancestor of the HIV-1 M group dates back to circa 1910. ^[243] Proponents of this dating link the HIV epidemic with the emergence of colonialism and growth of large colonial African cities, leading to social changes, including a higher degree of sexual promiscuity, the spread of prostitution, and the accompanying high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities. ^[244] While transmission rates of HIV during vaginal intercourse are low under regular circumstances, they are increased many fold if one of the partners suffers from a sexually transmitted infection causing genital ulcers. Early 1900s colonial cities were notable due to their high prevalence of prostitution and genital ulcers, to the degree that, as of 1928, as many as 45% of female residents of eastern Kinshasa were thought to have been prostitutes, and, as of 1933, around 15% of all residents of the same city had syphilis. ^[244]

An alternative view holds that unsafe medical practices in Africa after World War II, such as unsterile reuse of single use syringes during mass vaccination, antibiotic and anti-malaria treatment campaigns, were the initial vector that allowed the virus to adapt to humans and spread. ^{[242] [245] [246]}

The earliest well-documented case of HIV in a human dates back to 1959 in the Congo. ^[247] The earliest retrospectively described case of AIDS is believed to have been in Norway beginning in 1966. ^[248] In July 1960, in the wake of Congo's independence, the United Nations recruited Francophone experts and technicians from all over the world to assist in filling administrative gaps left by Belgium, who did not leave behind an African elite to run the country. By 1962, Haitians made up the second largest group of well-educated experts (out of the 48 national groups recruited), that totaled around 4500 in the country. ^{[249] [250]} Dr. Jacques Pépin, a Quebecer author of The Origins of AIDS, stipulates that Haiti was one of HIV's entry points to the United States and that one of them may have carried HIV back across the Atlantic in the 1960s. ^[250] Although the virus may have been present in the United States as early as 1966, ^[251] the vast majority of infections occurring outside sub-Saharan Africa (including the U.S.) can be traced back to a single unknown individual who became infected with HIV in Haiti and then brought the infection to the United States some time around 1969. ^[252] The epidemic then rapidly spread among high-risk groups (initially, sexually promiscuous men who have sex with men). By 1978, the prevalence of HIV-1 among homosexual male residents of New York City and San Francisco was estimated at 5%, suggesting that several thousand individuals in the country had been infected. ^[252]

Society and culture

Stigma

Main article: Discrimination against people with HIV/AIDS

Ryan White became a poster child for HIV after being expelled from school because he was infected.

AIDS stigma exists around the world in a variety of ways, including ostracism, rejection, discrimination and avoidance of HIV infected people; compulsory HIV testing without prior consent or protection of confidentiality; violence against HIV infected individuals or people who are perceived to be infected with HIV; and the quarantine of HIV infected individuals. ^[21] Stigma-related violence or the fear of violence prevents many people from seeking HIV testing, returning for their results, or securing treatment, possibly turning what could be a manageable chronic illness into a death sentence and perpetuating the spread of HIV. ^[254]

AIDS stigma has been further divided into the following three categories:

• Instrumental AIDS stigma—a reflection of the fear and apprehension that are likely to be associated with any deadly and transmissible illness. ^[255]
• Symbolic AIDS stigma—the use of HIV/AIDS to express attitudes toward the social groups or lifestyles perceived to be associated with the disease. ^[255]
• Courtesy AIDS stigma—stigmatization of people connected to the issue of HIV/AIDS or HIV-positive people. ^[256]

Often, AIDS stigma is expressed in conjunction with one or more other stigmas, particularly those associated with homosexuality, bisexuality, promiscuity, prostitution, and intravenous drug use. ^[257]

In many developed countries, there is an association between AIDS and homosexuality or bisexuality, and this association is correlated with higher levels of sexual prejudice, such as anti-homosexual/bisexual attitudes. ^[258] There is also a perceived association between AIDS and all male-male sexual behavior, including sex between uninfected men. ^[255] However, the dominant mode of spread worldwide for HIV remains heterosexual transmission. ^[259]

In 2003, as part of an overall reform of marriage and population legislation, it became legal for people with AIDS to marry in China. ^[260]

In 2013 the U.S. National Library of Medicine developed a traveling exhibition titled, "Surviving and Thriving: AIDS, Politics, and Culture", ^[261] covering medical research, U.S. government's response, and personal stories from people with AIDS, caregivers, and activists. ^[262]

Economic impact

Main articles: Economic impact of HIV/AIDS and Cost of HIV treatment

Changes in life expectancy in some African countries, 1960–2012

HIV/AIDS affects the economics of both individuals and countries. ^[214] The gross domestic product of the most affected countries has decreased due to the lack of human capital. ^{[214] [263]} Without proper nutrition, health care and medicine, large numbers of people die from AIDS-related complications. They will not only be unable to work, but will also require significant medical care. It is estimated that as of 2007 there were 12 million AIDS orphans. ^[214] Many are cared for by elderly grandparents. ^[264]

Returning to work after beginning treatment for HIV/AIDS is difficult, and affected people often work less than the average worker. Unemployment in people with HIV/AIDS also is associated with suicidal ideation, memory problems, and social isolation. Employment increases self-esteem, sense of dignity, confidence, and quality of life for people with HIV/AIDS. Anti-retroviral treatment may help people with HIV/AIDS work more, and may increase the chance that a person with HIV/AIDS will be employed (low quality evidence). ^[265]

By affecting mainly young adults, AIDS reduces the taxable population, in turn reducing the resources available for public expenditures such as education and health services not related to AIDS resulting in increasing pressure for the state's finances and slower growth of the economy. This causes a slower growth of the tax base, an effect that is reinforced if there are growing expenditures on treating the sick, training (to replace sick workers), sick pay and caring for AIDS orphans. This is especially true if the sharp increase in adult mortality shifts the responsibility and blame from the family to the government in caring for these orphans. ^[264]

At the household level, AIDS causes both loss of income and increased spending on healthcare. A study in Côte d'Ivoire showed that households having a person with HIV/AIDS spent twice as much on medical expenses as other households. This additional expenditure also leaves less income to spend on education and other personal or family investment. ^[266]

Religion and AIDS

Main article: Religion and HIV/AIDS

The topic of religion and AIDS has become highly controversial in the past twenty years, primarily because some religious authorities have publicly declared their opposition to the use of condoms. ^{[267] [268]} The religious approach to prevent the spread of AIDS according to a report by American health expert Matthew Hanley titled The Catholic Church and the Global AIDS Crisis argues that cultural changes are needed including a re-emphasis on fidelity within marriage and sexual abstinence outside of it. ^[268]

Some religious organizations have claimed that prayer can cure HIV/AIDS. In 2011, the BBC reported that some churches in London were claiming that prayer would cure AIDS, and the Hackney-based Centre for the Study of Sexual Health and HIV reported that several people stopped taking their medication, sometimes on the direct advice of their pastor, leading to a number of deaths. ^[269] The Synagogue Church Of All Nations advertised an "anointing water" to promote God's healing, although the group denies advising people to stop taking medication. ^[269]

Media portrayal

Main article: Media portrayal of HIV/AIDS

One of the first high-profile cases of AIDS was the American Rock Hudson, a gay actor who had been married and divorced earlier in life, who died on October 2, 1985 having announced that he was suffering from the virus on July 25 that year. He had been diagnosed during 1984. ^[270] A notable British casualty of AIDS that year was Nicholas Eden, a gay politician and son of the late prime minister Anthony Eden. ^[271] On November 24, 1991, the virus claimed the life of British rock star Freddie Mercury, lead singer of the band Queen, who died from an AIDS-related illness having only revealed the diagnosis on the previous day. ^[272] However, he had been diagnosed as HIV positive in 1987. ^[273] One of the first high-profile heterosexual cases of the virus was Arthur Ashe, the American tennis player. He was diagnosed as HIV positive on August 31, 1988, having contracted the virus from blood transfusions during heart surgery earlier in the 1980s. Further tests within 24 hours of the initial diagnosis revealed that Ashe had AIDS, but he did not tell the public about his diagnosis until April 1992. ^[274] He died as a result on February 6, 1993 at age 49. ^[275]

Therese Frare's photograph of gay activist David Kirby, as he lay dying from AIDS while surrounded by family, was taken in April 1990. LIFE magazine said the photo became the one image "most powerfully identified with the HIV/AIDS epidemic." The photo was displayed in LIFE magazine, was the winner of the World Press Photo, and acquired worldwide notoriety after being used in a United Colors of Benetton advertising campaign in 1992. ^[276] In 1996, Johnson Aziga, a Ugandan-born Canadian was diagnosed with HIV, but subsequently had unprotected sex with 11 women without disclosing his diagnosis. By 2003 seven had contracted HIV, and two died from complications related to AIDS. ^{[277] [278]} Aziga was convicted of first-degree murder and was sentenced for life. ^[279]

Criminal transmission

Main article: Criminal transmission of HIV

Criminal transmission of HIV is the intentional or reckless infection of a person with the human immunodeficiency virus (HIV). Some countries or jurisdictions, including some areas of the United States, have laws that criminalize HIV transmission or exposure. ^[280] Others may charge the accused under laws enacted before the HIV pandemic.

Misconceptions

Main articles: Misconceptions about HIV/AIDS and Discredited HIV/AIDS origins theories

There are many misconceptions about HIV and AIDS. Three of the most common are that AIDS can spread through casual contact, that sexual intercourse with a virgin will cure AIDS, ^{[281] [282] [283]} and that HIV can infect only gay men and drug users. In 2014, some among the British public wrongly thought one could get HIV from kissing (16%), sharing a glass (5%), spitting (16%), a public toilet seat (4%), and coughing or sneezing (5%). ^[284] Other misconceptions are that any act of anal intercourse between two uninfected gay men can lead to HIV infection, and that open discussion of HIV and homosexuality in schools will lead to increased rates of AIDS. ^{[285] [286]}

A small group of individuals continue to dispute the connection between HIV and AIDS, ^[287] the existence of HIV itself, or the validity of HIV testing and treatment methods. ^{[288] [289]} These claims, known as AIDS denialism, have been examined and rejected by the scientific community. ^[290] However, they have had a significant political impact, particularly in South Africa, where the government's official embrace of AIDS denialism (1999–2005) was responsible for its ineffective response to that country's AIDS epidemic, and has been blamed for hundreds of thousands of avoidable deaths and HIV infections. ^{[291] [292] [293]}

Several discredited conspiracy theories have held that HIV was created by scientists, either inadvertently or deliberately. Operation INFEKTION was a worldwide Soviet active measures operation to spread the claim that the United States had created HIV/AIDS. Surveys show that a significant number of people believed—and continue to believe—in such claims. ^[294]

Research

Main article: HIV/AIDS research

HIV/AIDS research includes all medical research which attempts to prevent, treat, or cure HIV/AIDS along with fundamental research about the nature of HIV as an infectious agent and AIDS as the disease caused by HIV.

Many governments and research institutions participate in HIV/AIDS research. This research includes behavioral health interventions such as sex education, and drug development, such as research into microbicides for sexually transmitted diseases, HIV vaccines, and antiretroviral drugs. Other medical research areas include the topics of pre-exposure prophylaxis, post-exposure prophylaxis, and circumcision and HIV. Public health officials, researchers, and programs can gain a more comprehensive picture of the barriers they face, and the efficacy of current approaches to HIV treatment and prevention, by tracking standard HIV indicators. ^[295] Use of common indicators is an increasing focus of development organizations and researchers. ^{[296] [297]}

References

1. "What Are HIV and AIDS? | HIV.gov". www.hiv.gov. U.S. Department of Health and Human Services (HHS). 2017-05-15. Retrieved 10 September 2017.
2. "HIV Classification: CDC and WHO Staging Systems | AIDS Education and Training Centers National Coordinating Resource Center (AETC NCRC)". aidsetc.org. AIDS Education and Training Center Program. Archived from the original on October 18, 2017. Retrieved September 10, 2017.
3. "Wear your red ribbon this World AIDS Day | UNAIDS". www.unaids.org. UNAIDS Secretariat. Retrieved 10 September 2017.
4. "HIV/AIDS Fact sheet N°360". WHO. November 2015. Archived from the original on February 17, 2016. Retrieved February 11, 2016.
5. "About HIV/AIDS". CDC. December 6, 2015. Retrieved February 11, 2016.
6. UNAIDS (May 18, 2012). "The quest for an HIV vaccine". Archived from the original on May 24, 2012.
7. UNAIDS, WHO (December 2007). "2007 AIDS epidemic update" (PDF). Archived from the original (PDF) on May 27, 2008. Retrieved March 12, 2008.
8. "Global summary of the AIDS epidemic 2016" (PDF). UNAIDS. UNAIDS. June 2017. Retrieved 10 September 2017.
9. Sepkowitz KA (June 2001). "AIDS – the first 20 years". The New England Journal of Medicine. 344 (23): 1764–72. doi:10.1056/NEJM200106073442306. PMID   11396444.
10. Krämer A, Kretzschmar M, Krickeberg K (2010). Modern infectious disease epidemiology concepts, methods, mathematical models, and public health (Online-Ausg. ed.). New York: Springer. p. 88. ISBN   978-0-387-93835-6.
11. Kirch W (2008). Encyclopedia of Public Health. New York: Springer. pp. 676–77. ISBN   978-1-4020-5613-0.
12. Rom WN, Markowitz SB, eds. (2007). Environmental and occupational medicine (4th ed.). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins. p. 745. ISBN   978-0-7817-6299-1.
13. "HIV and Its Transmission". Centers for Disease Control and Prevention. 2003. Archived from the original on February 4, 2005. Retrieved May 23, 2006.
14. Guideline on when to start antiretroviral therapy and on pre-exposure prophylaxis for HIV (PDF). WHO. 2015. p. 13. ISBN   978-92-4-150956-5. Archived (PDF) from the original on October 14, 2015.
15. "Fact sheet – Latest statistics on the status of the AIDS epidemic | UNAIDS". www.unaids.org. Archived from the original on July 13, 2017. Retrieved July 21, 2017.
16. "Global HIV and AIDS statistics". AVERT. 2015-07-16. Retrieved 2017-10-07.
17. "Fact sheet – Latest statistics on the status of the AIDS epidemic". www.unaids.org. UNAIDS. Retrieved 2018-03-16.
18. Kallings LO (March 2008). "The first postmodern pandemic: 25 years of HIV/ AIDS". Journal of Internal Medicine. 263 (3): 218–43. doi:10.1111/j.1365-2796.2007.01910.x. PMID   18205765.(subscription required)
19. Sharp PM, Hahn BH (September 2011). "Origins of HIV and the AIDS pandemic". Cold Spring Harbor Perspectives in Medicine. 1 (1): a006841. doi:10.1101/cshperspect.a006841. PMC   3234451 . PMID   22229120.
20. Gallo RC (October 2006). "A reflection on HIV/AIDS research after 25 years". Retrovirology. 3 (1): 72. doi:10.1186/1742-4690-3-72. PMC   1629027 . PMID   17054781.
21. "The impact of AIDS on people and societies" (PDF). 2006 Report on the global AIDS epidemic. UNAIDS. 2006. ISBN   978-92-9173-479-5.
22. Endersby, Jim (2016). "Myth Busters". Science. 351 (6268): 35. Bibcode:2016Sci...351...35E. doi:10.1126/science.aad2891. Archived from the original on February 22, 2016. Retrieved February 14, 2016.
23. McCullom, Rob (February 26, 2013). "An African Pope Won't Change the Vatican's Views on Condoms and AIDS". The Atlantic. Archived from the original on March 8, 2016. Retrieved February 14, 2016.
24. Harden, Victoria Angela (2012). AIDS at 30: A History. Potomac Books Inc. p. 324. ISBN   978-1-59797-294-9.
25. Mandell, Bennett, and Dolan (2010). Chapter 121.
26. WHO case definitions of HIV for surveillance and revised clinical staging and immunological classification of HIV-related disease in adults and children (PDF). Geneva: World Health Organization. 2007. pp. 6–16. ISBN   978-92-4-159562-9. Archived (PDF) from the original on October 31, 2013.
27. Diseases and disorders. Tarrytown, NY: Marshall Cavendish. 2008. p. 25. ISBN   978-0-7614-7771-6.
28. Mandell, Bennett, and Dolan (2010). Chapter 118.
29. Vogel M, Schwarze-Zander C, Wasmuth JC, Spengler U, Sauerbruch T, Rockstroh JK (July 2010). "The treatment of patients with HIV". Deutsches Arzteblatt International. 107 (28–29): 507–15, quiz 516. doi:10.3238/arztebl.2010.0507. PMC   2915483 . PMID   20703338.
30. Evian, Clive (2006). Primary HIV/AIDS care: a practical guide for primary health care personnel in a clinical and supportive setting (Updated 4th ed.). Houghton [South Africa]: Jacana. p. 29. ISBN   978-1-77009-198-6.
31. Charles B. Hicks, MD (2001). Jacques W. A. J. Reeders & Philip Charles Goodman, ed. Radiology of AIDS. Berlin [u.a.]: Springer. p. 19. ISBN   978-3-540-66510-6.
32. Elliott, Tom (2012). Lecture Notes: Medical Microbiology and Infection. John Wiley & Sons. p. 273. ISBN   978-1-118-37226-5.
33. Blankson JN (March 2010). "Control of HIV-1 replication in elite suppressors". Discovery Medicine. 9 (46): 261–66. PMID   20350494.
34. Walker BD (Aug–Sep 2007). "Elite control of HIV Infection: implications for vaccines and treatment". Topics in HIV Medicine. 15 (4): 134–36. PMID   17720999.
35. Holmes CB, Losina E, Walensky RP, Yazdanpanah Y, Freedberg KA (March 2003). "Review of human immunodeficiency virus type 1-related opportunistic infections in sub-Saharan Africa". Clinical Infectious Diseases. 36 (5): 652–62. doi:10.1086/367655. PMID   12594648.
36. Chu C, Selwyn PA (February 2011). "Complications of HIV infection: a systems-based approach". American Family Physician. 83 (4): 395–406. PMID   21322514.
37. Mandell, Bennett, and Dolan (2010). Chapter 169.
38. Mittal R, Rath S, Vemuganti GK (July 2013). "Ocular surface squamous neoplasia – Review of etio-pathogenesis and an update on clinico-pathological diagnosis". Saudi Journal of Ophthalmology. 27 (3): 177–86. doi:10.1016/j.sjopt.2013.07.002. PMC   3770226 . PMID   24227983.
39. "AIDS". MedlinePlus. A.D.A.M. Archived from the original on June 18, 2012. Retrieved June 14, 2012.
40. Sestak K (July 2005). "Chronic diarrhea and AIDS: insights into studies with non-human primates". Current HIV Research. 3 (3): 199–205. doi:10.2174/1570162054368084. PMID   16022653.
41. Murray ED, Buttner N, Price BH (2012). "Depression and Psychosis in Neurological Practice". In Bradley WG, Daroff RB, Fenichel GM, Jankovic J. Bradley's Neurology in Clinical Practice: Expert Consult – Online and Print, 6e (Bradley, Neurology in Clinical Practice e-dition 2v Set). 1 (6th ed.). Philadelphia: Elsevier/Saunders. p. 101. ISBN   978-1-4377-0434-1.
42. Smith DK, Grohskopf LA, Black RJ, Auerbach JD, Veronese F, Struble KA, Cheever L, Johnson M, Paxton LA, Onorato IM, Greenberg AE (21 January 2005). "Antiretroviral postexposure prophylaxis after sexual, injection-drug use, or other nonoccupational exposure to HIV in the United States: recommendations from the U.S. Department of Health and Human Services". MMWR. Recommendations and reports : Morbidity and mortality weekly report. Recommendations and reports / Centers for Disease Control. 54 (RR-2): 1–20. PMID   15660015.
43. Coovadia H (2004). "Antiretroviral agents—how best to protect infants from HIV and save their mothers from AIDS". N. Engl. J. Med. 351 (3): 289–292. doi:10.1056/NEJMe048128. PMID   15247337.
44. Kripke C (1 August 2007). "Antiretroviral prophylaxis for occupational exposure to HIV". American Family Physician. 76 (3): 375–6. PMID   17708137.
45. Dosekun O, Fox J (July 2010). "An overview of the relative risks of different sexual behaviours on HIV transmission". Current Opinion in HIV and AIDS. 5 (4): 291–7. doi:10.1097/COH.0b013e32833a88a3. PMID   20543603.
46. Cunha, Burke (2012). Antibiotic Essentials 2012 (11 ed.). Jones & Bartlett Publishers. p. 303. ISBN   9781449693831.
47. Boily MC, Baggaley RF, Wang L, Masse B, White RG, Hayes RJ, Alary M (February 2009). "Heterosexual risk of HIV-1 infection per sexual act: systematic review and meta-analysis of observational studies". The Lancet Infectious Diseases. 9 (2): 118–29. doi:10.1016/S1473-3099(09)70021-0. PMID   19179227.
48. Baggaley RF, White RG, Boily MC (December 2008). "Systematic review of orogenital HIV-1 transmission probabilities". International Journal of Epidemiology. 37 (6): 1255–65. doi:10.1093/ije/dyn151. PMC   2638872 . PMID   18664564.
49. Kripke C (August 2007). "Antiretroviral prophylaxis for occupational exposure to HIV". American Family Physician. 76 (3): 375–76. PMID   17708137.
50. van der Kuyl AC, Cornelissen M (September 2007). "Identifying HIV-1 dual infections". Retrovirology. 4: 67. doi:10.1186/1742-4690-4-67. PMC   2045676 . PMID   17892568.
51. McCray, Eugene; Mermin, Jonathan (September 27, 2017). "Dear Colleague: September 27, 2017". Division of HIV/AIDS Prevention. Centers for Disease Control and Prevention. Retrieved February 1, 2018.
52. LeMessurier, J; Traversy, G; Varsaneux, O; Weekes, M; Avey, MT; Niragira, O; Gervais, R; Guyatt, G; Rodin, R (19 November 2018). "Risk of sexual transmission of human immunodeficiency virus with antiretroviral therapy, suppressed viral load and condom use: a systematic review". CMAJ : Canadian Medical Association Journal = Journal de l'Association Medicale Canadienne. 190 (46): E1350–E1360. doi:10.1503/cmaj.180311. PMC   6239917 . PMID   30455270.
53. "HIV Among Gay and Bisexual Men" (PDF). Archived (PDF) from the original on December 18, 2016. Retrieved January 1, 2017.
54. "Today's HIV/AIDS Epidemic Factsheet" (PDF). Centers for Disease Control and Prevention. Archived (PDF) from the original on December 19, 2016. Retrieved December 31, 2016.
55. Boily MC, Baggaley RF, Wang L, Masse B, White RG, Hayes RJ, Alary M (February 2009). "Heterosexual risk of HIV-1 infection per sexual act: systematic review and meta-analysis of observational studies". The Lancet. Infectious Diseases. 9 (2): 118–29. doi:10.1016/S1473-3099(09)70021-0. PMC   4467783 . PMID   19179227.
56. Beyrer C, Baral SD, van Griensven F, Goodreau SM, Chariyalertsak S, Wirtz AL, Brookmeyer R (July 2012). "Global epidemiology of HIV infection in men who have sex with men". Lancet. 380 (9839): 367–77. doi:10.1016/S0140-6736(12)60821-6. PMC   3805037 . PMID   22819660.
57. Yu M, Vajdy M (August 2010). "Mucosal HIV transmission and vaccination strategies through oral compared with vaginal and rectal routes". Expert Opinion on Biological Therapy. 10 (8): 1181–95. doi:10.1517/14712598.2010.496776. PMC   2904634 . PMID   20624114.
58. Stürchler, Dieter A. (2006). Exposure a guide to sources of infections. Washington, DC: ASM Press. p. 544. ISBN   978-1-55581-376-5.
59. Pattman R, et al., eds. (2010). Oxford handbook of genitourinary medicine, HIV, and sexual health (2nd ed.). Oxford: Oxford University Press. p. 95. ISBN   978-0-19-957166-6.
60. Dosekun O, Fox J (July 2010). "An overview of the relative risks of different sexual behaviours on HIV transmission". Current Opinion in HIV and AIDS. 5 (4): 291–97. doi:10.1097/COH.0b013e32833a88a3. PMID   20543603.
61. Ng BE, Butler LM, Horvath T, Rutherford GW (March 2011). Butler LM, ed. "Population-based biomedical sexually transmitted infection control interventions for reducing HIV infection". The Cochrane Database of Systematic Reviews (3): CD001220. doi:10.1002/14651858.CD001220.pub3. PMID   21412869.
62. Anderson J (February 2012). "Women and HIV: motherhood and more". Current Opinion in Infectious Diseases. 25 (1): 58–65. doi:10.1097/QCO.0b013e32834ef514. PMID   22156896.
63. Kerrigan, Deanna (2012). The Global HIV Epidemics among Sex Workers. World Bank Publications. p. 1–5. ISBN   978-0-8213-9775-6.
64. Aral, Sevgi (2013). The New Public Health and STD/HIV Prevention: Personal, Public and Health Systems Approaches. Springer. p. 120. ISBN   978-1-4614-4526-5.
65. Klimas N, Koneru AO, Fletcher MA (June 2008). "Overview of HIV". Psychosomatic Medicine. 70 (5): 523–30. doi:10.1097/PSY.0b013e31817ae69f. PMID   18541903.
66. Draughon JE, Sheridan DJ (2012). "Nonoccupational postexposure prophylaxis following sexual assault in industrialized low-HIV-prevalence countries: a review". Psychology, Health & Medicine. 17 (2): 235–54. doi:10.1080/13548506.2011.579984. PMID   22372741.
67. Baggaley RF, Boily MC, White RG, Alary M (April 2006). "Risk of HIV-1 transmission for parenteral exposure and blood transfusion: a systematic review and meta-analysis". AIDS. 20 (6): 805–12. doi:10.1097/01.aids.0000218543.46963.6d. PMID   16549963.
68. "HIV in the United States: An Overview". Center for Disease Control and Prevention. March 2012. Archived from the original on May 1, 2013.
69. "Will I need a blood transfusion?" (PDF). NHS patient information. National Health Services. 2011. Archived (PDF) from the original on October 25, 2012. Retrieved August 29, 2012.
70. Centers for Disease Control Prevention (CDC) (October 2010). "HIV transmission through transfusion – Missouri and Colorado, 2008". MMWR. Morbidity and Mortality Weekly Report. 59 (41): 1335–39. PMID   20966896.
71. UNAIDS 2011 pg. 60–70
72. "Blood safety ... for too few". WHO. 2001. Archived from the original on January 17, 2005.
73. Simonds RJ (November 1993). "HIV transmission by organ and tissue transplantation". AIDS. 7 Suppl 2: S35–38. doi:10.1097/00002030-199311002-00008. PMID   8161444.
74. Reid SR (August 2009). "Injection drug use, unsafe medical injections, and HIV in Africa: a systematic review". Harm Reduction Journal. 6: 24. doi:10.1186/1477-7517-6-24. PMC   2741434 . PMID   19715601.
75. "Basic Information about HIV and AIDS". Center for Disease Control and Prevention. April 2012. Archived from the original on June 18, 2017.
76. Crans, Wayne J. (June 1, 2010). "Why Mosquitoes Cannot Transmit AIDS". rci.rutgers.edu. Rutgers University. New Jersey Agricultural Experiment Station Publication No. H-40101-01-93. Archived from the original on March 29, 2014. Retrieved March 29, 2014.
77. "Preventing Mother-to-Child Transmission of HIV". HIV.gov. Retrieved 2017-12-08.
78. Coutsoudis A, Kwaan L, Thomson M (October 2010). "Prevention of vertical transmission of HIV-1 in resource-limited settings". Expert Review of Anti-Infective Therapy. 8 (10): 1163–75. doi:10.1586/eri.10.94. PMID   20954881.
79. Thorne C, Newell ML (June 2007). "HIV". Seminars in Fetal & Neonatal Medicine. 12 (3): 174–81. doi:10.1016/j.siny.2007.01.009. PMID   17321814.
80. White AB, Mirjahangir JF, Horvath H, Anglemyer A, Read JS (October 2014). "Antiretroviral interventions for preventing breast milk transmission of HIV". The Cochrane Database of Systematic Reviews. 10 (10): CD011323. doi:10.1002/14651858.CD011323. PMID   25280769.
81. "Infant feeding in the context of HIV". www.who.int. April 2011. Archived from the original on March 9, 2017. Retrieved March 9, 2017.
82. Cunningham, F, Leveno KJ, Bloom SL, Spong CY, Dashe JS, Hoffman BL, Casey BM, Sheffield JS (2013). "Abortion". Williams Obstetrics. McGraw-Hill. p. 5.
83. Alimonti JB, Ball TB, Fowke KR (July 2003). "Mechanisms of CD4+ T lymphocyte cell death in human immunodeficiency virus infection and AIDS". The Journal of General Virology. 84 (Pt 7): 1649–61. doi:10.1099/vir.0.19110-0. PMID   12810858.
84. International Committee on Taxonomy of Viruses (2002). "61.0.6. Lentivirus". National Institutes of Health. Archived from the original on April 18, 2006. Retrieved June 25, 2012.
85. International Committee on Taxonomy of Viruses (2002). "61. Retroviridae". National Institutes of Health. Archived from the original on December 17, 2001. Retrieved June 25, 2012.
86. Levy JA (November 1993). "HIV pathogenesis and long-term survival". AIDS. 7 (11): 1401–10. doi:10.1097/00002030-199311000-00001. PMID   8280406.
87. Smith JA, Daniel R (May 2006). "Following the path of the virus: the exploitation of host DNA repair mechanisms by retroviruses". ACS Chemical Biology. 1 (4): 217–26. doi:10.1021/cb600131q. PMID   17163676.
88. Martínez MA, ed. (2010). RNA interference and viruses : current innovations and future trends. Norfolk: Caister Academic Press. p. 73. ISBN   978-1-904455-56-1.
89. Gerald B. Pier, ed. (2004). Immunology, infection, and immunity. Washington, DC: ASM Press. p. 550. ISBN   978-1-55581-246-1.
90. Zhang C, Zhou S, Groppelli E, Pellegrino P, Williams I, Borrow P, Chain BM, Jolly C (April 2015). "Hybrid spreading mechanisms and T cell activation shape the dynamics of HIV-1 infection". PLoS Computational Biology. 11 (4): e1004179. arXiv: 1503.08992 . Bibcode:2015PLSCB..11E4179Z. doi:10.1371/journal.pcbi.1004179. PMC   4383537 . PMID   25837979.
91. Jolly C, Kashefi K, Hollinshead M, Sattentau QJ (January 2004). "HIV-1 cell to cell transfer across an Env-induced, actin-dependent synapse". The Journal of Experimental Medicine. 199 (2): 283–93. doi:10.1084/jem.20030648. PMC   2211771 . PMID   14734528.
92. Sattentau Q (November 2008). "Avoiding the void: cell-to-cell spread of human viruses". Nature Reviews. Microbiology. 6 (11): 815–26. doi:10.1038/nrmicro1972. PMID   18923409.
93. Sigal A, Kim JT, Balazs AB, Dekel E, Mayo A, Milo R, Baltimore D (August 2011). "Cell-to-cell spread of HIV permits ongoing replication despite antiretroviral therapy". Nature. 477 (7362): 95–98. Bibcode:2011Natur.477...95S. doi:10.1038/nature10347. PMID   21849975.
94. Gilbert PB, McKeague IW, Eisen G, Mullins C, Guéye-NDiaye A, Mboup S, Kanki PJ (February 2003). "Comparison of HIV-1 and HIV-2 infectivity from a prospective cohort study in Senegal". Statistics in Medicine. 22 (4): 573–93. doi:10.1002/sim.1342. PMID   12590415.
95. Reeves JD, Doms RW (June 2002). "Human immunodeficiency virus type 2". The Journal of General Virology. 83 (Pt 6): 1253–65. doi:10.1099/0022-1317-83-6-1253. PMID   12029140.
96. Piatak M, Saag MS, Yang LC, Clark SJ, Kappes JC, Luk KC, Hahn BH, Shaw GM, Lifson JD (March 1993). "High levels of HIV-1 in plasma during all stages of infection determined by competitive PCR". Science. 259 (5102): 1749–54. Bibcode:1993Sci...259.1749P. doi:10.1126/science.8096089. PMID   8096089.
97. Pantaleo G, Demarest JF, Schacker T, Vaccarezza M, Cohen OJ, Daucher M, Graziosi C, Schnittman SS, Quinn TC, Shaw GM, Perrin L, Tambussi G, Lazzarin A, Sekaly RP, Soudeyns H, Corey L, Fauci AS (January 1997). "The qualitative nature of the primary immune response to HIV infection is a prognosticator of disease progression independent of the initial level of plasma viremia". Proceedings of the National Academy of Sciences of the United States of America. 94 (1): 254–58. Bibcode:1997PNAS...94..254P. doi:10.1073/pnas.94.1.254. PMC   19306 . PMID   8990195.
98. Hel Z, McGhee JR, Mestecky J (June 2006). "HIV infection: first battle decides the war". Trends in Immunology. 27 (6): 274–81. doi:10.1016/j.it.2006.04.007. PMID   16679064.
99. Pillay, Deenan; Genetti, Anna Maria; Weiss, Robin A. (2007). "Human Immunodeficiency Viruses". In Zuckerman, Arie J.; et al. Principles and practice of clinical virology (6th ed.). Hoboken, NJ: Wiley. p. 905. ISBN   978-0-470-51799-4.
100. Mehandru S, Poles MA, Tenner-Racz K, Horowitz A, Hurley A, Hogan C, Boden D, Racz P, Markowitz M (September 2004). "Primary HIV-1 infection is associated with preferential depletion of CD4+ T lymphocytes from effector sites in the gastrointestinal tract". The Journal of Experimental Medicine. 200 (6): 761–70. doi:10.1084/jem.20041196. PMC   2211967 . PMID   15365095.
101. Brenchley JM, Schacker TW, Ruff LE, Price DA, Taylor JH, Beilman GJ, Nguyen PL, Khoruts A, Larson M, Haase AT, Douek DC (September 2004). "CD4+ T cell depletion during all stages of HIV disease occurs predominantly in the gastrointestinal tract". The Journal of Experimental Medicine. 200 (6): 749–59. doi:10.1084/jem.20040874. PMC   2211962 . PMID   15365096.
102. Olson WC, Jacobson JM (March 2009). "CCR5 monoclonal antibodies for HIV-1 therapy". Current Opinion in HIV and AIDS. 4 (2): 104–11. doi:10.1097/COH.0b013e3283224015. PMC   2760828 . PMID   19339948.
103. editor, Julio Aliberti (2011). Control of Innate and Adaptive Immune Responses During Infectious Diseases. New York: Springer Verlag. p. 145. ISBN   978-1-4614-0483-5.
104. Appay V, Sauce D (January 2008). "Immune activation and inflammation in HIV-1 infection: causes and consequences". The Journal of Pathology. 214 (2): 231–41. doi:10.1002/path.2276. PMID   18161758.
105. Brenchley JM, Price DA, Schacker TW, Asher TE, Silvestri G, Rao S, Kazzaz Z, Bornstein E, Lambotte O, Altmann D, Blazar BR, Rodriguez B, Teixeira-Johnson L, Landay A, Martin JN, Hecht FM, Picker LJ, Lederman MM, Deeks SG, Douek DC (December 2006). "Microbial translocation is a cause of systemic immune activation in chronic HIV infection". Nature Medicine. 12 (12): 1365–71. doi:10.1038/nm1511. PMC   1717013 . PMID   17115046.
106. "HIV/AIDS Testing". CDC. 16 March 2018. Retrieved 14 April 2018.
107. Moyer VA (July 2013). "Screening for HIV: U.S. Preventive Services Task Force Recommendation Statement". Annals of Internal Medicine. 159 (1): 51–60. doi:10.7326/0003-4819-159-1-201307020-00645. PMID   23698354.
108. Kellerman S, Essajee S (July 2010). "HIV testing for children in resource-limited settings: what are we waiting for?". PLoS Medicine. 7 (7): e1000285. doi:10.1371/journal.pmed.1000285. PMC   2907270 . PMID   20652012.
109. UNAIDS 2011 pg. 70–80
110. Schneider E, Whitmore S, Glynn KM, Dominguez K, Mitsch A, McKenna MT (December 2008). "Revised surveillance case definitions for HIV infection among adults, adolescents, and children aged <18 months and for HIV infection and AIDS among children aged 18 months to <13 years – United States, 2008". MMWR. Recommendations and Reports. 57 (RR-10): 1–12. PMID   19052530.
111. Centers for Disease Control Prevention (CDC) (April 2014). "Revised surveillance case definition for HIV infection – United States, 2014". MMWR. Recommendations and Reports. 63 (RR-03): 1–10. PMID   24717910.
112. Crosby R, Bounse S (March 2012). "Condom effectiveness: where are we now?". Sexual Health. 9 (1): 10–17. doi:10.1071/SH11036. PMID   22348628.
113. "Condom Facts and Figures". WHO. August 2003. Archived from the original on October 18, 2012. Retrieved January 17, 2006.
114. Gallo MF, Kilbourne-Brook M, Coffey PS (March 2012). "A review of the effectiveness and acceptability of the female condom for dual protection". Sexual Health. 9 (1): 18–26. doi:10.1071/SH11037. PMID   22348629.
115. Celum C, Baeten JM (February 2012). "Tenofovir-based pre-exposure prophylaxis for HIV prevention: evolving evidence". Current Opinion in Infectious Diseases. 25 (1): 51–57. doi:10.1097/QCO.0b013e32834ef5ef. PMC   3266126 . PMID   22156901.
116. Baptista M, Ramalho-Santos J (November 2009). "Spermicides, microbicides and antiviral agents: recent advances in the development of novel multi-functional compounds". Mini Reviews in Medicinal Chemistry. 9 (13): 1556–67. doi:10.2174/138955709790361548. PMID   20205637.
117. Siegfried N, Muller M, Deeks JJ, Volmink J (April 2009). Siegfried N, ed. "Male circumcision for prevention of heterosexual acquisition of HIV in men". The Cochrane Database of Systematic Reviews (2): CD003362. doi:10.1002/14651858.CD003362.pub2. PMID   19370585.
118. "WHO and UNAIDS announce recommendations from expert consultation on male circumcision for HIV prevention". World Health Organization. March 28, 2007. Archived from the original on July 3, 2011.
119. Larke N (May 27, 2010). "Male circumcision, HIV and sexually transmitted infections: a review". British Journal of Nursing. 19 (10): 629–34. doi:10.12968/bjon.2010.19.10.48201. PMC   3836228 . PMID   20622758.
120. Eaton L, Kalichman SC (November 2009). "Behavioral aspects of male circumcision for the prevention of HIV infection". Current HIV/AIDS Reports. 6 (4): 187–93. doi:10.1007/s11904-009-0025-9. PMC   3557929 . PMID   19849961.(subscription required)
121. Kim HH, Li PS, Goldstein M (November 2010). "Male circumcision: Africa and beyond?". Current Opinion in Urology. 20 (6): 515–19. doi:10.1097/MOU.0b013e32833f1b21. PMID   20844437.
122. Templeton DJ, Millett GA, Grulich AE (February 2010). "Male circumcision to reduce the risk of HIV and sexually transmitted infections among men who have sex with men". Current Opinion in Infectious Diseases. 23 (1): 45–52. doi:10.1097/QCO.0b013e328334e54d. PMID   19935420.
123. Wiysonge CS, Kongnyuy EJ, Shey M, Muula AS, Navti OB, Akl EA, Lo YR (June 2011). Wiysonge CS, ed. "Male circumcision for prevention of homosexual acquisition of HIV in men". The Cochrane Database of Systematic Reviews (6): CD007496. doi:10.1002/14651858.CD007496.pub2. PMID   21678366.
124. Marrazzo JM, del Rio C, Holtgrave DR, Cohen MS, Kalichman SC, Mayer KH, Montaner JS, Wheeler DP, Grant RM, Grinsztejn B, Kumarasamy N, Shoptaw S, Walensky RP, Dabis F, Sugarman J, Benson CA (Jul 23–30, 2014). "HIV prevention in clinical care settings: 2014 recommendations of the International Antiviral Society–USA Panel". JAMA. 312 (4): 390–409. doi:10.1001/jama.2014.7999. PMC   6309682 . PMID   25038358.
125. Eaton LA, Kalichman S (December 2007). "Risk compensation in HIV prevention: implications for vaccines, microbicides, and other biomedical HIV prevention technologies". Current HIV/AIDS Reports. 4 (4): 165–72. doi:10.1007/s11904-007-0024-7. PMC   2937204 . PMID   18366947.
126. Underhill K, Operario D, Montgomery P (October 2007). Operario D, ed. "Abstinence-only programs for HIV infection prevention in high-income countries". The Cochrane Database of Systematic Reviews (4): CD005421. doi:10.1002/14651858.CD005421.pub2. PMID   17943855. Archived from the original on November 25, 2010.
127. Tolli MV (October 2012). "Effectiveness of peer education interventions for HIV prevention, adolescent pregnancy prevention and sexual health promotion for young people: a systematic review of European studies". Health Education Research. 27 (5): 904–13. doi:10.1093/her/cys055. PMID   22641791.
128. Ljubojević S, Lipozenčić J (2010). "Sexually transmitted infections and adolescence". Acta Dermatovenerologica Croatica. 18 (4): 305–10. PMID   21251451.
129. International technical guidance on sexuality education: an evidence-informed approach (PDF). Paris: UNESCO. 2018. p. 12. ISBN   978-92-3-100259-5.
130. Patel VL, Yoskowitz NA, Kaufman DR, Shortliffe EH (September 2008). "Discerning patterns of human immunodeficiency virus risk in healthy young adults". The American Journal of Medicine. 121 (9): 758–64. doi:10.1016/j.amjmed.2008.04.022. PMC   2597652 . PMID   18724961.
131. Fonner VA, Denison J, Kennedy CE, O'Reilly K, Sweat M (September 2012). "Voluntary counseling and testing (VCT) for changing HIV-related risk behavior in developing countries". The Cochrane Database of Systematic Reviews. 9 (9): CD001224. doi:10.1002/14651858.CD001224.pub4. PMC   3931252 . PMID   22972050.
132. Anglemyer A, Rutherford GW, Horvath T, Baggaley RC, Egger M, Siegfried N (April 2013). "Antiretroviral therapy for prevention of HIV transmission in HIV-discordant couples". The Cochrane Database of Systematic Reviews. 4 (4): CD009153. doi:10.1002/14651858.CD009153.pub3. PMC   4026368 . PMID   23633367.
133. Chou R, Selph S, Dana T, Bougatsos C, Zakher B, Blazina I, Korthuis PT (November 2012). "Screening for HIV: systematic review to update the 2005 U.S. Preventive Services Task Force recommendation". Annals of Internal Medicine. 157 (10): 706–18. doi:10.7326/0003-4819-157-10-201211200-00007. PMID   23165662.
134. Choopanya K, Martin M, Suntharasamai P, Sangkum U, Mock PA, Leethochawalit M, Chiamwongpaet S, Kitisin P, Natrujirote P, Kittimunkong S, Chuachoowong R, Gvetadze RJ, McNicholl JM, Paxton LA, Curlin ME, Hendrix CW, Vanichseni S (June 2013). "Antiretroviral prophylaxis for HIV infection in injecting drug users in Bangkok, Thailand (the Bangkok Tenofovir Study): a randomised, double-blind, placebo-controlled phase 3 trial". Lancet. 381 (9883): 2083–90. doi:10.1016/S0140-6736(13)61127-7. PMID   23769234.
135. "Draft Recommendation Statement: Prevention of Human Immunodeficiency Virus (HIV) Infection: Pre-Exposure Prophylaxis – US Preventive Services Task Force". www.uspreventiveservicestaskforce.org. Retrieved 21 November 2018.
136. Centers for Disease Control (CDC) (August 1987). "Recommendations for prevention of HIV transmission in health-care settings". MMWR Supplements. 36 (2): 1S–18S. PMID   3112554. Archived from the original on July 9, 2017.
137. Kurth AE, Celum C, Baeten JM, Vermund SH, Wasserheit JN (March 2011). "Combination HIV prevention: significance, challenges, and opportunities". Current HIV/AIDS Reports. 8 (1): 62–72. doi:10.1007/s11904-010-0063-3. PMC   3036787 . PMID   20941553.
138. MacArthur GJ, Minozzi S, Martin N, Vickerman P, Deren S, Bruneau J, Degenhardt L, Hickman M (October 2012). "Opiate substitution treatment and HIV transmission in people who inject drugs: systematic review and meta-analysis". BMJ. 345 (oct03 3): e5945. doi:10.1136/bmj.e5945. PMC   3489107 . PMID   23038795.
139. "HIV exposure through contact with body fluids". Prescrire International. 21 (126): 100–01, 103–05. April 2012. PMID   22515138.
140. Kuhar DT, Henderson DK, Struble KA, Heneine W, Thomas V, Cheever LW, Gomaa A, Panlilio AL (September 2013). "Updated US Public Health Service guidelines for the management of occupational exposures to human immunodeficiency virus and recommendations for postexposure prophylaxis". Infection Control and Hospital Epidemiology. 34 (9): 875–92. doi:10.1086/672271. PMID   23917901.
141. Linden JA (September 2011). "Clinical practice. Care of the adult patient after sexual assault". The New England Journal of Medicine. 365 (9): 834–41. doi:10.1056/NEJMcp1102869. PMID   21879901.
142. Young TN, Arens FJ, Kennedy GE, Laurie JW, Rutherford GW (January 2007). Young T, ed. "Antiretroviral post-exposure prophylaxis (PEP) for occupational HIV exposure". The Cochrane Database of Systematic Reviews (1): CD002835. doi:10.1002/14651858.CD002835.pub3. PMID   17253483.
143. Siegfried N, van der Merwe L, Brocklehurst P, Sint TT (July 2011). Siegfried N, ed. "Antiretrovirals for reducing the risk of mother-to-child transmission of HIV infection". The Cochrane Database of Systematic Reviews (7): CD003510. doi:10.1002/14651858.CD003510.pub3. PMID   21735394.
144. "WHO HIV and Infant Feeding Technical Consultation Held on behalf of the Inter-agency Task Team (IATT) on Prevention of HIV – Infections in Pregnant Women, Mothers and their Infants – Consensus statement" (PDF). October 25–27, 2006. Archived (PDF) from the original on April 9, 2008. Retrieved March 12, 2008.
145. Horvath T, Madi BC, Iuppa IM, Kennedy GE, Rutherford G, Read JS (January 2009). Horvath T, ed. "Interventions for preventing late postnatal mother-to-child transmission of HIV". The Cochrane Database of Systematic Reviews (1): CD006734. doi:10.1002/14651858.CD006734.pub2. PMID   19160297.
146. "WHO validates elimination of mother-to-child transmission of HIV and syphilis in Cuba". WHO. June 30, 2015. Archived from the original on September 4, 2015. Retrieved August 30, 2015.
147. Reynell L, Trkola A (March 2012). "HIV vaccines: an attainable goal?". Swiss Medical Weekly. 142: w13535. doi:10.4414/smw.2012.13535. PMID   22389197.
148. U.S. Army Office of the Surgeon General (March 21, 2011). "HIV Vaccine Trial in Thai Adults". ClinicalTrials.gov. Archived from the original on October 19, 2011. Retrieved June 28, 2011.
149. U.S. Army Office of the Surgeon General (June 2, 2010). "Follow up of Thai Adult Volunteers With Breakthrough HIV Infection After Participation in a Preventive HIV Vaccine Trial". ClinicalTrials.gov. Archived from the original on June 9, 2012.
150. May MT, Ingle SM (December 2011). "Life expectancy of HIV-positive adults: a review". Sexual Health. 8 (4): 526–33. doi:10.1071/SH11046. PMID   22127039.
151. UNAIDS 2011 pg. 1–10
152. Antiretroviral therapy for HIV infection in adults and adolescents: recommendations for a public health approach (PDF). World Health Organization. 2010. pp. 19–20. ISBN   978-92-4-159976-4. Archived (PDF) from the original on July 9, 2012.
153. Consolidated guidelines on the use of antiretroviral drugs for treating and preventing HIV infection (PDF). World Health Organization. 2013. pp. 28–30. ISBN   978-92-4-150572-7. Archived (PDF) from the original on February 9, 2014.
154. "Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents" (PDF). Department of Health and Human Services. February 12, 2013. p. i. Archived (PDF) from the original on November 1, 2016. Retrieved January 3, 2014.
155. Sterne JA, May M, Costagliola D, de Wolf F, Phillips AN, Harris R, Funk MJ, Geskus RB, Gill J, Dabis F, Miró JM, Justice AC, Ledergerber B, Fätkenheuer G, Hogg RS, Monforte AD, Saag M, Smith C, Staszewski S, Egger M, Cole SR (April 2009). "Timing of initiation of antiretroviral therapy in AIDS-free HIV-1-infected patients: a collaborative analysis of 18 HIV cohort studies". Lancet. 373 (9672): 1352–63. doi:10.1016/S0140-6736(09)60612-7. PMC   2670965 . PMID   19361855.
156. Beard J, Feeley F, Rosen S (November 2009). "Economic and quality of life outcomes of antiretroviral therapy for HIV/AIDS in developing countries: a systematic literature review". AIDS Care. 21 (11): 1343–56. doi:10.1080/09540120902889926. PMID   20024710.
157. Attia S, Egger M, Müller M, Zwahlen M, Low N (July 2009). "Sexual transmission of HIV according to viral load and antiretroviral therapy: systematic review and meta-analysis". AIDS. 23 (11): 1397–404. doi:10.1097/QAD.0b013e32832b7dca. PMID   19381076.
158. Orrell C (November 2005). "Antiretroviral adherence in a resource-poor setting". Current HIV/AIDS Reports. 2 (4): 171–76. doi:10.1007/s11904-005-0012-8. PMID   16343374.
159. Malta M, Strathdee SA, Magnanini MM, Bastos FI (August 2008). "Adherence to antiretroviral therapy for human immunodeficiency virus/acquired immune deficiency syndrome among drug users: a systematic review". Addiction. 103 (8): 1242–57. doi:10.1111/j.1360-0443.2008.02269.x. PMID   18855813.
160. Nachega JB, Marconi VC, van Zyl GU, Gardner EM, Preiser W, Hong SY, Mills EJ, Gross R (April 2011). "HIV treatment adherence, drug resistance, virologic failure: evolving concepts". Infectious Disorders Drug Targets. 11 (2): 167–74. doi:10.2174/187152611795589663. PMC   5072419 . PMID   21406048.
161. Orsi F, d'almeida C (May 2010). "Soaring antiretroviral prices, TRIPS and TRIPS flexibilities: a burning issue for antiretroviral treatment scale-up in developing countries". Current Opinion in HIV and AIDS. 5 (3): 237–41. doi:10.1097/COH.0b013e32833860ba. PMID   20539080.
162. Nachega JB, Mills EJ, Schechter M (January 2010). "Antiretroviral therapy adherence and retention in care in middle-income and low-income countries: current status of knowledge and research priorities". Current Opinion in HIV and AIDS. 5 (1): 70–77. doi:10.1097/COH.0b013e328333ad61. PMID   20046150.
163. Montessori V, Press N, Harris M, Akagi L, Montaner JS (January 2004). "Adverse effects of antiretroviral therapy for HIV infection". Canadian Medical Association Journal. 170 (2): 229–38. PMC   315530 . PMID   14734438.
164. Burgoyne RW, Tan DH (March 2008). "Prolongation and quality of life for HIV-infected adults treated with highly active antiretroviral therapy (HAART): a balancing act". The Journal of Antimicrobial Chemotherapy. 61 (3): 469–73. doi:10.1093/jac/dkm499. PMID   18174196.
165. Barbaro G, Barbarini G (December 2011). "Human immunodeficiency virus & cardiovascular risk". The Indian Journal of Medical Research. 134 (6): 898–903. doi:10.4103/0971-5916.92634. PMC   3284097 . PMID   22310821.
166. "Summary of recommendations on when to start ART in children" (PDF). Consolidated ARV guidelines, June 2013. June 2013. Archived (PDF) from the original on October 18, 2014.
167. "Guidelines for the Use of Antiretroviral Agents in Pediatric HIV Infection" (PDF). Department of Health and Human Services, February 2014. March 2014. Archived (PDF) from the original on September 14, 2015.
168. "Guidelines for intensified tuberculosis case-finding and isoniazid preventive therapy for people living with HIV in resource-constrained settings" (PDF). Department of HIV/AIDS, World Health Organization 2011. 2011. Archived (PDF) from the original on October 19, 2014.
169. Laurence J (January 2006). "Hepatitis A and B virus immunization in HIV-infected persons". The AIDS Reader. 16 (1): 15–17. PMID   16433468.
170. UNAIDS 2011 pg. 150–160
171. Huang L, Cattamanchi A, Davis JL, den Boon S, Kovacs J, Meshnick S, Miller RF, Walzer PD, Worodria W, Masur H (June 2011). "HIV-associated Pneumocystis pneumonia". Proceedings of the American Thoracic Society. 8 (3): 294–300. doi:10.1513/pats.201009-062WR. PMC   3132788 . PMID   21653531.
172. "Treating opportunistic infections among HIV-infected adults and adolescents. Recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association/Infectious Diseases Society of America". Department of Health and Human Services. February 2, 2007. Retrieved 26 July 2018.
173. Smith, Blaine T., ed. (2008). Concepts in immunology and immunotherapeutics (4th ed.). Bethesda, MD: American Society of Health-System Pharmacists. p. 143. ISBN   978-1-58528-127-5.
174. Beck CR, McKenzie BC, Hashim AB, Harris RC, Zanuzdana A, Agboado G, et al. (September 2013). "Influenza vaccination for immunocompromised patients: summary of a systematic review and meta-analysis". Influenza and Other Respiratory Viruses. 7 Suppl 2: 72–75. doi:10.1111/irv.12084. PMC   5909396 . PMID   24034488.
175. Lee KY, Tsai MS, Kuo KC, Tsai JC, Sun HY, Cheng AC, Chang SY, Lee CH, Hung CC (2014). "Pneumococcal vaccination among HIV-infected adult patients in the era of combination antiretroviral therapy". Human Vaccines & Immunotherapeutics. 10 (12): 3700–10. doi:10.4161/hv.32247. PMC   4514044 . PMID   25483681.
176. World Health Organization (May 2003). Nutrient requirements for people living with HIV/AIDS: Report of a technical consultation (PDF). Geneva. Archived (PDF) from the original on March 25, 2009. Retrieved March 31, 2009.
177. Forrester JE, Sztam KA (December 2011). "Micronutrients in HIV/AIDS: is there evidence to change the WHO 2003 recommendations?". The American Journal of Clinical Nutrition. 94 (6): 1683S–1689S. doi:10.3945/ajcn.111.011999. PMC   3226021 . PMID   22089440.
178. Nunnari G, Coco C, Pinzone MR, Pavone P, Berretta M, Di Rosa M, Schnell M, Calabrese G, Cacopardo B (June 2012). "The role of micronutrients in the diet of HIV-1-infected individuals". Frontiers in Bioscience. 4: 2442–56. PMID   22652651. Archived from the original on April 16, 2015.
179. Zeng L, Zhang L (December 2011). "Efficacy and safety of zinc supplementation for adults, children and pregnant women with HIV infection: systematic review". Tropical Medicine & International Health. 16 (12): 1474–82. doi:10.1111/j.1365-3156.2011.02871.x. PMID   21895892.
180. Visser ME, Durao S, Sinclair D, Irlam JH, Siegfried N (May 2017). "Micronutrient supplementation in adults with HIV infection". The Cochrane Database of Systematic Reviews. 5: CD003650. doi:10.1002/14651858.CD003650.pub4. PMC   5458097 . PMID   28518221.
181. Stone CA, Kawai K, Kupka R, Fawzi WW (November 2010). "Role of selenium in HIV infection". Nutrition Reviews. 68 (11): 671–81. doi:10.1111/j.1753-4887.2010.00337.x. PMC   3066516 . PMID   20961297.
182. Siegfried N, Irlam JH, Visser ME, Rollins NN (March 2012). "Micronutrient supplementation in pregnant women with HIV infection". The Cochrane Database of Systematic Reviews (3): CD009755. doi:10.1002/14651858.CD009755. PMID   22419344.
183. Irlam JH, Siegfried N, Visser ME, Rollins NC (October 2013). "Micronutrient supplementation for children with HIV infection". The Cochrane Database of Systematic Reviews (10): CD010666. doi:10.1002/14651858.CD010666. PMID   24114375.
184. Littlewood RA, Vanable PA (September 2008). "Complementary and alternative medicine use among HIV-positive people: research synthesis and implications for HIV care". AIDS Care. 20 (8): 1002–18. doi:10.1080/09540120701767216. PMC   2570227 . PMID   18608078.
185. Mills E, Wu P, Ernst E (June 2005). "Complementary therapies for the treatment of HIV: in search of the evidence". International Journal of STD & AIDS. 16 (6): 395–403. doi:10.1258/0956462054093962. PMID   15969772.
186. Liu JP, Manheimer E, Yang M (July 2005). Liu JP, ed. "Herbal medicines for treating HIV infection and AIDS". The Cochrane Database of Systematic Reviews (3): CD003937. doi:10.1002/14651858.CD003937.pub2. PMID   16034917.
187. Lutge EE, Gray A, Siegfried N (April 2013). "The medical use of cannabis for reducing morbidity and mortality in patients with HIV/AIDS". The Cochrane Database of Systematic Reviews. 4 (4): CD005175. doi:10.1002/14651858.CD005175.pub3. PMID   23633327.
188. Knoll B, Lassmann B, Temesgen Z (December 2007). "Current status of HIV infection: a review for non-HIV-treating physicians". International Journal of Dermatology. 46 (12): 1219–28. doi:10.1111/j.1365-4632.2007.03520.x. PMID   18173512.
189. Morgan D, Mahe C, Mayanja B, Okongo JM, Lubega R, Whitworth JA (March 2002). "HIV-1 infection in rural Africa: is there a difference in median time to AIDS and survival compared with that in industrialized countries?". AIDS. 16 (4): 597–603. doi:10.1097/00002030-200203080-00011. PMID   11873003.
190. Zwahlen M, Egger M (2006). "Progression and mortality of untreated HIV-positive individuals living in resource-limited settings: update of literature review and evidence synthesis" (PDF). UNAIDS Obligation HQ/05/422204. Archived (PDF) from the original on April 9, 2008. Retrieved March 19, 2008.
191. Antiretroviral Therapy Cohort Collaboration (July 2008). "Life expectancy of individuals on combination antiretroviral therapy in high-income countries: a collaborative analysis of 14 cohort studies". Lancet. 372 (9635): 293–99. doi:10.1016/S0140-6736(08)61113-7. PMC   3130543 . PMID   18657708.
192. Schackman BR, Gebo KA, Walensky RP, Losina E, Muccio T, Sax PE, Weinstein MC, Seage GR, Moore RD, Freedberg KA (November 2006). "The lifetime cost of current human immunodeficiency virus care in the United States". Medical Care. 44 (11): 990–97. doi:10.1097/01.mlr.0000228021.89490.2a. PMID   17063130.
193. van Sighem AI, Gras LA, Reiss P, Brinkman K, de Wolf F (June 2010). "Life expectancy of recently diagnosed asymptomatic HIV-infected patients approaches that of uninfected individuals". AIDS. 24 (10): 1527–35. doi:10.1097/QAD.0b013e32833a3946. PMID   20467289.
194. Cheung MC, Pantanowitz L, Dezube BJ (Jun–Jul 2005). "AIDS-related malignancies: emerging challenges in the era of highly active antiretroviral therapy". The Oncologist. 10 (6): 412–26. doi:10.1634/theoncologist.10-6-412. PMID   15967835.
195. Tang J, Kaslow RA (2003). "The impact of host genetics on HIV infection and disease progression in the era of highly active antiretroviral therapy". AIDS. 17 Suppl 4 (Suppl 4): S51–60. doi:10.1097/00002030-200317004-00006. PMID   15080180.
196. Lawn SD (January 2004). "AIDS in Africa: the impact of coinfections on the pathogenesis of HIV-1 infection". The Journal of Infection. 48 (1): 1–12. doi:10.1016/j.jinf.2003.09.001. PMID   14667787.
197. Campbell GR, Pasquier E, Watkins J, Bourgarel-Rey V, Peyrot V, Esquieu D, Barbier P, de Mareuil J, Braguer D, Kaleebu P, Yirrell DL, Loret EP (November 2004). "The glutamine-rich region of the HIV-1 Tat protein is involved in T-cell apoptosis". The Journal of Biological Chemistry. 279 (46): 48197–204. doi:10.1074/jbc.M406195200. PMID   15331610.
198. Campbell GR, Watkins JD, Esquieu D, Pasquier E, Loret EP, Spector SA (November 2005). "The C terminus of HIV-1 Tat modulates the extent of CD178-mediated apoptosis of T cells". The Journal of Biological Chemistry. 280 (46): 38376–82. doi:10.1074/jbc.M506630200. PMID   16155003.
199. "Tuberculosis". Fact sheet 104. World Health Organization. March 2012. Archived from the original on August 23, 2012. Retrieved August 29, 2012.
200. World Health Organization (2011). Global tuberculosis control 2011 (PDF). ISBN   978-92-4-156438-0. Archived from the original (PDF) on September 6, 2012. Retrieved August 29, 2012.
201. Rubin R, Strayer DS, Rubin E, eds. (2011). Rubin's pathology : clinicopathologic foundations of medicine (Sixth ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 154. ISBN   978-1-60547-968-2.
202. Nelson VM, Benson AB (January 2017). "Epidemiology of Anal Canal Cancer". Surgical Oncology Clinics of North America. 26 (1): 9–15. doi:10.1016/j.soc.2016.07.001. PMID   27889039.
203. Woods SP, Moore DJ, Weber E, Grant I (June 2009). "Cognitive neuropsychology of HIV-associated neurocognitive disorders". Neuropsychology Review. 19 (2): 152–68. doi:10.1007/s11065-009-9102-5. PMC   2690857 . PMID   19462243.
204. Brown TT, Qaqish RB (November 2006). "Antiretroviral therapy and the prevalence of osteopenia and osteoporosis: a meta-analytic review". AIDS. 20 (17): 2165–74. doi:10.1097/QAD.0b013e32801022eb. PMID   17086056.
205. Nicholas PK, Kemppainen JK, Canaval GE, Corless IB, Sefcik EF, Nokes KM, Bain CA, Kirksey KM, Eller LS, Dole PJ, Hamilton MJ, Coleman CL, Holzemer WL, Reynolds NR, Portillo CJ, Bunch EH, Wantland DJ, Voss J, Phillips R, Tsai YF, Mendez MR, Lindgren TG, Davis SM, Gallagher DM (February 2007). "Symptom management and self-care for peripheral neuropathy in HIV/AIDS". AIDS Care. 19 (2): 179–89. doi:10.1080/09540120600971083. PMID   17364396.
206. Boshoff C, Weiss R (May 2002). "AIDS-related malignancies". Nature Reviews. Cancer. 2 (5): 373–82. doi:10.1038/nrc797. PMID   12044013.
207. Yarchoan R, Tosato G, Little RF (August 2005). "Therapy insight: AIDS-related malignancies – the influence of antiviral therapy on pathogenesis and management". Nature Clinical Practice Oncology. 2 (8): 406–15, quiz 423. doi:10.1038/ncponc0253. PMID   16130937.
208. Post FA, Holt SG (February 2009). "Recent developments in HIV and the kidney". Current Opinion in Infectious Diseases. 22 (1): 43–48. doi:10.1097/QCO.0b013e328320ffec. PMID   19106702.
209. "AIDSinfo". UNAIDS. Archived from the original on March 5, 2013. Retrieved March 4, 2013.
210. Cohen MS, Hellmann N, Levy JA, DeCock K, Lange J (April 2008). "The spread, treatment, and prevention of HIV-1: evolution of a global pandemic". The Journal of Clinical Investigation. 118 (4): 1244–54. doi:10.1172/JCI34706. PMC   2276790 . PMID   18382737.
211. "UNAIDS reports a 52% reduction in new HIV infections among children and a combined 33% reduction among adults and children since 2001". UNAIDS. Archived from the original on October 1, 2013. Retrieved October 7, 2013.
212. UNAIDS 2011 pg. 20–30
213. UNAIDS 2011 pp. 40–50
214. Mandell, Bennett, and Dolan (2010). Chapter 117.
215. New HIV infections among children have been reduced by 50% or more in seven countries in sub-Saharan Africa Archived June 30, 2013, at the Wayback Machine , UN AIDS, Geneva, June 25, 2013.
216. Centers for Disease Control Prevention (CDC) (June 2011). "HIV surveillance – United States, 1981–2008". MMWR. Morbidity and Mortality Weekly Report. 60 (21): 689–93. PMID   21637182.
217. Public Health England (2016). HIV in the United Kingdom: 2016 Report (PDF). Archived (PDF) from the original on April 25, 2017.
218. Surveillance; riques, Risk Assessment Division = Le VIH et le sida au Canada: rapport de surveillance en date du 31 décembre 2009 / Division de la surveillance et de l'évaluation des (2010). HIV and AIDS in Canada : surveillance report to December 31, 2009 (PDF). Ottawa: Public Health Agency of Canada, Centre for Communicable Diseases and Infection Control, Surveillance and Risk Assessment Division. ISBN   978-1-100-52141-1. Archived from the original (PDF) on January 19, 2012.
219. "Global Report Fact Sheet" (PDF). UNAIDS. 2010. Archived from the original (PDF) on March 19, 2013.
220. "Country Comparison :: HIV/AIDS – Adult Prevalence Rate". CIA World Factbook. Archived from the original on December 21, 2014. Retrieved November 6, 2014.
221. "'How I told the world about Aids'". BBC News. 5 June 2006. Retrieved 12 February 2019.
222. Gottlieb MS (June 2006). "Pneumocystis pneumonia – Los Angeles. 1981". American Journal of Public Health. 96 (6): 980–81, discussion 982–83. doi:10.2105/AJPH.96.6.980. PMC   1470612 . PMID   16714472. Archived from the original on April 22, 2009.
223. Friedman-Kien AE (October 1981). "Disseminated Kaposi's sarcoma syndrome in young homosexual men". Journal of the American Academy of Dermatology. 5 (4): 468–71. doi:10.1016/S0190-9622(81)80010-2. PMID   7287964.
224. Hymes KB, Cheung T, Greene JB, Prose NS, Marcus A, Ballard H, William DC, Laubenstein LJ (September 1981). "Kaposi's sarcoma in homosexual men-a report of eight cases". Lancet. 2 (8247): 598–600. doi:10.1016/S0140-6736(81)92740-9. PMID   6116083.
225. Basavapathruni A, Anderson KS (December 2007). "Reverse transcription of the HIV-1 pandemic". FASEB Journal. 21 (14): 3795–808. doi:10.1096/fj.07-8697rev. PMID   17639073.
226. Centers for Disease Control (CDC) (May 1982). "Persistent, generalized lymphadenopathy among homosexual males". MMWR. Morbidity and Mortality Weekly Report. 31 (19): 249–51. PMID   6808340. Archived from the original on October 18, 2011.
227. Barré-Sinoussi F, Chermann JC, Rey F, Nugeyre MT, Chamaret S, Gruest J, Dauguet C, Axler-Blin C, Vézinet-Brun F, Rouzioux C, Rozenbaum W, Montagnier L (May 1983). "Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS)". Science. 220 (4599): 868–71. Bibcode:1983Sci...220..868B. doi:10.1126/science.6189183. PMID   6189183.
228. Centers for Disease Control (CDC) (July 1982). "Opportunistic infections and Kaposi's sarcoma among Haitians in the United States". MMWR. Morbidity and Mortality Weekly Report. 31 (26): 353–54, 360–61. PMID   6811853. Archived from the original on September 20, 2011.
229. Gilman, Sander L (1987). Gilman, Sander L., ed. "AIDS and Syphilis: The Iconography of Disease". October. 43: 87–107. doi:10.2307/3397566. JSTOR   3397566.
230. "Making Headway Under Hellacious Circumstances" (PDF). American Association for the Advancement of Science. July 28, 2006. Archived (PDF) from the original on June 24, 2008. Retrieved June 23, 2008.
231. Altman LK (May 11, 1982). "New homosexual disorder worries health officials". The New York Times. Archived from the original on April 30, 2013. Retrieved August 31, 2011.