Acquired immune deficiency syndrome or acquired immunodeficiency syndrome (AIDS) is a disease of the human immune system caused by the human immunodeficiency virus (HIV).[1] The illness interferes with the immune system, making people with AIDS much more likely to get infections, including opportunistic infections and tumors that do not affect people with working immune systems. This susceptibility gets worse as the disease continues.
HIV is transmitted in a number of ways including: sexual intercourse (including oral sex and anal sex); contaminated blood transfusions and hypodermic needles; and exchange between mother and baby during pregnancy, childbirth, and breastfeeding. It can be transmitted by any contact of a mucous membrane or the bloodstream with a bodily fluid that has the virus in it, such as the blood, semen, vaginal fluid, preseminal fluid, or breast milk from an infected person.[2][3]
Although treatments for HIV/AIDS can slow the course of the disease, there is no known cure or HIV vaccine. Antiretroviral treatment reduces both the deaths and new infections from HIV/AIDS, but these drugs are expensive and the medications are not available in all countries.[4] Due to the difficulty in treating HIV infection, preventing infection is a key aim in controlling the AIDS pandemic, with health organizations promoting safe sex and needle-exchange programmes in attempts to slow the spread of the virus. The virus and disease are often referred to together as HIV/AIDS. The disease is a major health problem in many parts of the world, and is considered a pandemic, a disease outbreak that is not only present over a large area but is actively spreading.[5] In 2009, the World Health Organization (WHO) estimated that there are 33.4 million people worldwide living with HIV/AIDS, with 2.7 million new HIV infections per year and 2.0 million annual deaths due to AIDS.[6] As of 2010 approximately 34 million people have HIV globally.[7] Of these approximately 16.8 million are women and 3.4 million are less than 15 years old.[7] It results in about 1.8 million death from AIDS in 2010 down from 3.1 million in 2001.[7] Since AIDS was first recognized in 1981 and 2009 it has led to nearly 30 million deaths.[8]
Genetic research indicates that HIV originated in west-central Africa during the late nineteenth or early twentieth century.[9][10] AIDS was first recognized by the Centers for Disease Control and Prevention (CDC) in 1981 and its cause, HIV, identified in the early 1980s.[11]
The symptoms of AIDS are primarily the result of conditions that do not normally develop in individuals with healthy immune systems. Most of these conditions are opportunistic infections caused by bacteria, viruses, fungi and parasites that are normally controlled by the elements of the immune system that HIV damages.[12] These infections affect nearly every organ system.
People with AIDS also have an increased risk of developing various cancers such as Kaposi's sarcoma, cervical cancer and cancers of the immune system known as lymphomas. Additionally, people with AIDS often have systemic symptoms of infection like fevers, sweats (particularly at night), swollen glands, chills, weakness, and weight loss.[13][14] The specific opportunistic infections that AIDS patients develop depend in part on the prevalence of these infections in the geographic area in which the patient lives.
Pneumocystis pneumonia (PCP) (originally known as Pneumocystis carinii pneumonia) is relatively rare in healthy, immunocompetent people, but common among HIV-infected individuals. It is caused by Pneumocystis jirovecii.
Before the advent of effective diagnosis, treatment and routine prophylaxis in Western countries, it was a common immediate cause of death. In developing countries, it is still one of the first indications of AIDS in untested individuals, although it does not generally occur unless the CD4 count is less than 200 cells per µL of blood.[15]
Tuberculosis (TB) is unique among infections associated with HIV because it is transmissible to immunocompetent people via the respiratory route, and is not easily treatable once identified.[16] Multidrug resistance is a serious problem. Tuberculosis with HIV co-infection (TB/HIV) is a major world health problem according to the World Health Organization: in 2007, 456,000 deaths among incident TB cases were HIV-positive, a third of all TB deaths and nearly a quarter of the estimated 2 million HIV deaths in that year.[17] Even though its incidence has declined because of the use of directly observed therapy and other improved practices in Western countries, this is not the case in developing countries where HIV is most prevalent. In early-stage HIV infection (CD4 count >300 cells per µL), TB typically presents as a pulmonary disease. In advanced HIV infection, TB often presents atypically with extrapulmonary (systemic) disease a common feature. Symptoms are usually constitutional and are not localized to one particular site, often affecting bone marrow, bone, urinary and gastrointestinal tracts, liver, regional lymph nodes, and the central nervous system.[18]
Esophagitis is an inflammation of the lining of the lower end of the esophagus (gullet or swallowing tube leading to the stomach). In HIV-infected individuals, this is normally due to fungal (candidiasis) or viral (herpes simplex-1 or cytomegalovirus) infections. In rare cases, it could be due to mycobacteria.[19]
Unexplained chronic diarrhea in HIV infection is due to many possible causes, including common bacterial (Salmonella, Shigella, Listeria or Campylobacter) and parasitic infections; and uncommon opportunistic infections such as cryptosporidiosis, microsporidiosis, Mycobacterium avium complex (MAC) and viruses,[20] astrovirus, adenovirus, rotavirus and cytomegalovirus, (the latter as a course of colitis).
In some cases, diarrhea may be a side effect of several drugs used to treat HIV, or it may simply accompany HIV infection, particularly during primary HIV infection. It may also be a side effect of antibiotics used to treat bacterial causes of diarrhea (common for Clostridium difficile). In the later stages of HIV infection, diarrhea is thought to be a reflection of changes in the way the intestinal tract absorbs nutrients, and may be an important component of HIV-related wasting.[21]
HIV infection may lead to a variety of neuropsychiatric sequelae, either by infection of the now susceptible nervous system by organisms, or as a direct consequence of the illness itself.[22]
Toxoplasmosis is a disease caused by the single-celled parasite called Toxoplasma gondii; it usually infects the brain, causing toxoplasma encephalitis, but it can also infect and cause disease in the eyes and lungs.[23] Cryptococcal meningitis is an infection of the meninx (the membrane covering the brain and spinal cord) by the fungus Cryptococcus neoformans. It can cause fevers, headache, fatigue, nausea, and vomiting. Patients may also develop seizures and confusion; left untreated, it can be lethal.
Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease, in which the gradual destruction of the myelin sheath covering the axons of nerve cells impairs the transmission of nerve impulses. It is caused by a virus called JC virus which occurs in 70% of the population in latent form, causing disease only when the immune system has been severely weakened, as is the case for AIDS patients. It progresses rapidly, usually causing death within months of diagnosis.[24]
AIDS dementia complex (ADC) is a metabolic encephalopathy induced by HIV infection and fueled by immune activation of HIV infected brain macrophages and microglia. These cells are productively infected by HIV and secrete neurotoxins of both host and viral origin.[25] Specific neurological impairments are manifested by cognitive, behavioral, and motor abnormalities that occur after years of HIV infection and are associated with low CD4+ T cell levels and high plasma viral loads.
Prevalence is 10–20% in Western countries[26] but only 1–2% of HIV infections in India.[27][28] This difference is possibly due to the HIV subtype in India. AIDS related mania is sometimes seen in patients with advanced HIV illness; it presents with more irritability and cognitive impairment and less euphoria than a manic episode associated with true bipolar disorder. Unlike the latter condition, it may have a more chronic course. This syndrome is less frequently seen with the advent of multi-drug therapy.
People with HIV infections have substantially increased incidence of several cancers. This is primarily due to co-infection with an oncogenic DNA virus, especially Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV) (also known as human herpesvirus-8 [HHV-8]), and human papillomavirus (HPV).[29][30]
Kaposi's sarcoma (KS) is the most common tumor in HIV-infected patients. The appearance of this tumor in young homosexual men in 1981 was one of the first signals of the AIDS epidemic. Caused by a gammaherpes virus called Kaposi's sarcoma-associated herpes virus (KSHV), it often appears as purplish nodules on the skin, but can affect other organs, especially the mouth, gastrointestinal tract, and lungs. High-grade B cell lymphomas such as Burkitt's lymphoma, Burkitt's-like lymphoma, diffuse large B-cell lymphoma (DLBCL), and primary central nervous system lymphoma present more often in HIV-infected patients. These particular cancers often foreshadow a poor prognosis. Epstein-Barr virus (EBV) or KSHV cause many of these lymphomas. In HIV-infected patients, lymphoma often arises in extranodal sites such as the gastrointestinal tract.[31] When they occur in an HIV-infected patient, KS and aggressive B cell lymphomas confer a diagnosis of AIDS.
Invasive cervical cancer in HIV-infected women is also considered AIDS-defining, it is caused by human papillomavirus (HPV).[32]
In addition to the AIDS-defining tumors listed above, HIV-infected patients are at increased risk of certain other tumors, notably Hodgkin's disease, anal and rectal carcinomas, hepatocellular carcinomas, head and neck cancers, and lung cancer. Some of these are causes by viruses, such as Hodgkin's disease (EBV), anal/rectal cancers (HPV), head and neck cancers (HPV), and hepatocellular carcinoma (hepatitis B or C). Other contributing factors include exposure to carcinogens (cigarette smoke for lung cancer), or living for years with subtle immune defects.
Interestingly, the incidence of many common tumors, such as breast cancer or colon cancer, does not increase in HIV-infected patients. In areas where HAART is extensively used to treat AIDS, the incidence of many AIDS-related malignancies has decreased, but at the same time malignant cancers overall have become the most common cause of death of HIV-infected patients.[33] In recent years, an increasing proportion of these deaths have been from non-AIDS-defining cancers.
People with AIDS often develop opportunistic infections that present with non-specific symptoms, especially low-grade fevers and weight loss. These include opportunistic infection with Mycobacterium avium-intracellulare and cytomegalovirus (CMV). CMV can cause colitis, as described above, and CMV retinitis can cause blindness.
Penicilliosis due to Penicillium marneffei is now the third most common opportunistic infection (after extrapulmonary tuberculosis and cryptococcosis) in HIV-positive individuals within the endemic area of Southeast Asia.[34]
An infection that often goes unrecognized in people with AIDS is Parvovirus B19. Its main consequence is anemia, which is difficult to distinguish from the effects of antiretroviral drugs used to treat AIDS itself.[35]
For more details on this topic, see
HIV.
AIDS is the ultimate clinical consequence of infection with HIV. HIV is a retrovirus that primarily infects vital organs of the human immune system such as CD4+ T cells (a subset of T cells), macrophages and dendritic cells. It directly and indirectly destroys CD4+ T cells.[36]
Once the number of CD4+ T cells per microliter (µL) of blood drops below 200, cellular immunity is lost. Acute HIV infection usually progresses over time to clinical latent HIV infection and then to early symptomatic HIV infection and later to AIDS, which is identified either on the basis of the amount of CD4+ T cells remaining in the blood, and/or the presence of certain infections, as noted above.[37]
In the absence of antiretroviral therapy, the median time of progression from HIV infection to AIDS is nine to ten years, and the median survival time after developing AIDS is only 9.2 months.[38] However, the rate of clinical disease progression varies widely between individuals, from two weeks up to 20 years.
Many factors affect the rate of progression. These include factors that influence the body's ability to defend against HIV such as the infected person's general immune function.[39][40] Older people have weaker immune systems, and therefore have a greater risk of rapid disease progression than younger people.
Poor access to health care and the existence of coexisting infections such as tuberculosis also may predispose people to faster disease progression.[38][41][42] The infected person's genetic inheritance plays an important role and some people are resistant to certain strains of HIV. An example of this is people with the homozygous CCR5-Δ32 variation are resistant to infection with certain strains of HIV.[43] HIV is genetically variable and exists as different strains, which cause different rates of clinical disease progression.[44][45][46]
The three main transmission routes of HIV are sexual contact, exposure to infected body fluids or tissues, and from mother to fetus or child during the perinatal period. It is possible to find HIV in the saliva, tears, and urine of infected individuals, but there are no recorded cases of infection by these secretions, and the risk of infection is negligible.[47]
Average per act risk for acquisition
of HIV by exposure route to an infected source
| Exposure Route |
Chance of infection |
| Blood Transfusion |
90% [48] |
| Childbirth (to child) |
25%[49] |
| Needle-sharing injection drug use |
0.67%[48] |
| Percutaneous needle stick |
0.30%[50] |
| Receptive anal intercourse* |
0.04–3.0%[51] |
| Insertive anal intercourse* |
0.06–0.056%[51] |
| Receptive penile-vaginal intercourse* |
0.05–0.30%[51][52] |
| Insertive penile-vaginal intercourse* |
0.01–0.38% [51][52] |
| Receptive oral intercourse*§ |
0–0.04% [51] |
| Insertive oral intercourse*§ |
0-0.005%[53] |
* assuming no condom use
§ source refers to oral intercourse
performed on a man |
Sexual transmission occurs with the contact between sexual secretions of one person with the rectal, genital or oral mucous membranes of another. Unprotected sexual acts are riskier for the receptive partner than for the insertive partner, and the risk for transmitting HIV through unprotected anal intercourse is greater than the risk from vaginal intercourse or oral sex.
The majority of HIV infections are acquired through unprotected sexual relations between partners, one of whom has HIV. The primary mode of HIV infection worldwide is through sexual contact between members of the opposite sex.[54][55][56]
However, oral sex is not entirely safe, as HIV can be transmitted through both insertive and receptive oral sex.[57][58] Sexual assault greatly increases the risk of HIV transmission as condoms are rarely employed and physical trauma to the vagina or rectum occurs frequently, facilitating the transmission of HIV.[59]
Other sexually transmitted infections (STI) increase the risk of HIV transmission and infection, because they cause the disruption of the normal epithelial barrier by genital ulceration and/or microulceration; and by accumulation of pools of HIV-susceptible or HIV-infected cells (lymphocytes and macrophages) in semen and vaginal secretions. Epidemiological studies from sub-Saharan Africa, Europe and North America suggest that genital ulcers, such as those caused by syphilis and/or chancroid, increase the risk of becoming infected with HIV by about fourfold. There is also a significant although lesser increase in risk from STIs such as gonorrhea, chlamydia and trichomoniasis, which all cause local accumulations of lymphocytes and macrophages.[60]
Transmission of HIV depends on the infectiousness of the index case and the susceptibility of the uninfected partner. Infectivity seems to vary during the course of illness and is not constant between individuals. An undetectable plasma viral load does not necessarily indicate a low viral load in the seminal liquid or genital secretions. People who have been infected with one strain of HIV can still be infected later on in their lives by other strains.
Infection is unlikely in a single encounter. High rates of infection have been linked to a pattern of overlapping long-term sexual relationships. This allows the virus to quickly spread to multiple partners who in turn infect their partners. A pattern of serial monogamy or occasional casual encounters is associated with lower rates of infection.[61]
CDC poster from 1989 highlighting the threat of AIDS associated with drug use
This transmission route is particularly relevant to intravenous drug users, hemophiliacs and recipients of blood transfusions and blood products. Sharing and reusing syringes contaminated with HIV-infected blood represents a major risk for infection with HIV.
Needle sharing is the cause of one third of all new HIV-infections in North America, China, and Eastern Europe. This route can also affect people who give and receive tattoos and piercings. Universal precautions are frequently not followed in both sub-Saharan Africa and much of Asia because of both a shortage of supplies and inadequate training.
The WHO estimates that approximately 2.5% of all HIV infections in sub-Saharan Africa are transmitted through unsafe healthcare injections.[62] Because of this, the United Nations General Assembly has urged the nations of the world to implement precautions to prevent HIV transmission by health workers.[63]
The risk of aquiring HIV from a blood blood transfusion is extremely low in developed countries where improved donor selection and HIV screening is performed. However, according to the WHO, the overwhelming majority of the world's population do not have access to safe blood and between 5% and 10% of the world's HIV infections come from transfusion of infected blood and blood products.[64]
The risk of acquiring HIV from a needle stick from an HIV-infected person is about 0.3% (~1 in 333) and the risk post mucus membrane exposure to infected blood is 0.09% (~1:1000).[50]
The transmission of the virus from the mother to the child can occur in utero during the last weeks of pregnancy and at childbirth. In the absence of treatment, the transmission rate between a mother and her child during pregnancy, labor and delivery is 25%.
However, when the mother takes antiretroviral therapy and gives birth by caesarean section, the rate of transmission is just 1%.[49] The risk of infection is influenced by the viral load of the mother at birth, with the higher the viral load, the higher the risk. Breastfeeding also increases the risk of transmission by about 4 %.[65]
There is no risk of acquiring HIV if exposed to feces, nasal secretions, saliva, sputum, sweat, tears, urine, or vomit from an HIV infected person unless these are contaminated with blood.[50]
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, and that HIV can infect only homosexual men and drug users. Other misconceptions are that any act of anal intercourse between two uninfected gay men can lead to HIV infection, and that open discussion of homosexuality and HIV in schools will lead to increased rates of homosexuality and AIDS.[66][67]
The pathophysiology of AIDS is complex.[68] Ultimately, HIV causes AIDS by depleting CD4+ T helper lymphocytes. This weakens the immune system and allows opportunistic infections. T lymphocytes 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.[69]
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.
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.[70] The reason for the preferential loss of mucosal CD4+ T cells is that a majority of mucosal CD4+ T cells express the CCR5 coreceptor, whereas a small fraction of CD4+ T cells in the bloodstream do so.[71]
HIV seeks out and destroys CCR5 expressing CD4+ cells during acute infection. A vigorous immune response eventually controls the infection and initiates the clinically latent phase. However, CD4+ T cells in mucosal tissues remain depleted throughout the infection, although enough remain to initially ward off life-threatening infections.
Continuous HIV replication results in a state of generalized immune activation persisting throughout the chronic phase.[72] Immune activation, which is reflected by the increased activation state of immune cells and release of proinflammatory cytokines, results from the activity of several HIV gene products and the immune response to ongoing HIV replication. Another cause is the breakdown of the immune surveillance system of the mucosal barrier caused by the depletion of mucosal CD4+ T cells during the acute phase of disease.[73]
This results in the systemic exposure of the immune system to microbial components of the gut’s normal flora, which in a healthy person is kept in check by the mucosal immune system. The activation and proliferation of T cells that results from immune activation provides fresh targets for HIV infection. However, direct killing by HIV alone cannot account for the observed depletion of CD4+ T cells since only 0.01–0.10% of CD4+ T cells in the blood are infected.
A major cause of CD4+ T cell loss appears to result from their heightened susceptibility to apoptosis when the immune system remains activated. Although new T cells are continuously produced by the thymus to replace the ones lost, the regenerative capacity of the thymus is slowly destroyed by direct infection of its thymocytes by HIV. Eventually, the minimal number of CD4+ T cells necessary to maintain a sufficient immune response is lost, leading to AIDS.
A generalized graph of the relationship between HIV copies (viral load) and CD4 counts over the average course of untreated HIV infection; any particular individual's disease course may vary considerably.
CD4+ T Lymphocyte count (cells/mm³) HIV RNA copies per mL of plasma
The diagnosis of AIDS in a person infected with HIV is based on the presence of certain signs or symptoms. Since June 5, 1981, many definitions have been developed for epidemiological surveillance such as the Bangui definition and the 1994 expanded World Health Organization AIDS case definition. However, clinical staging of patients was not an intended use for these systems as they are neither sensitive, nor specific. In developing countries, the World Health Organization's staging system for HIV infection and disease is used (using clinical and laboratory data), and in developed countries the CDC's classification system is used.
In 1990, the World Health Organization (WHO) grouped these infections and conditions together by introducing a staging system for people infected with HIV-1.[74] An update took place in September 2005. Most of these conditions are opportunistic infections that are easily treatable in healthy people.
There are two main definitions for AIDS. The older definition is to referring to AIDS using the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus.[75][76] In 1993, the CDC expanded their definition of AIDS to include all HIV positive people with a CD4+ T cell count below 200 per µL of blood or 14% of all lymphocytes.[77] The majority of new AIDS cases in developed countries use either this definition or the pre-1993 CDC definition. 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.
Many people are unaware that they are infected with HIV.[78] Less than 1% of the sexually active urban population in Africa has been tested, and this proportion is even lower in rural populations. Furthermore, only 0.5% of pregnant women attending urban health facilities are counseled, tested or receive their test results. Again, this proportion is even lower in rural health facilities.[78] Therefore, donor blood and blood products used in medicine and medical research are screened for HIV.
HIV tests are usually performed on venous blood. Many laboratories use fourth generation screening tests which detect anti-HIV antibody (IgG and IgM) and the HIV p24 antigen. The detection of HIV antibody or antigen in a patient previously known to be negative is evidence of HIV infection. Individuals whose first specimen indicates evidence of HIV infection will have a repeat test on a second blood sample to confirm the results.
The window period (the time between initial infection and the development of detectable antibodies against the infection) can vary since it can take 3–6 months to seroconvert and to test positive. Detection of the virus using polymerase chain reaction (PCR) during the window period is possible, and evidence suggests that an infection may often be detected earlier than when using a fourth generation EIA screening test.
Positive results obtained by PCR are confirmed by antibody tests.[79] Routinely used HIV tests for infection in neonates and infants (i. e., patients younger than 2 years),[80] born to HIV-positive mothers, have no value because of the presence of maternal antibody to HIV in the child's blood. HIV infection can only be diagnosed by PCR, testing for HIV pro-viral DNA in the children's lymphocytes.[81]
AIDS Clinic,
McLeod Ganj, Himachel Pradesh, India, 2010
Consistent condom use reduces the risk of heterosexual HIV transmission by approximately 80% over the long-term.[82] Where one partner of a couple is infected, consistent condom use results in rates of HIV infection for the uninfected person of below 1% per year.[83] Some data supports the equivalence of female condoms to latex condoms however the evidence is not definitive.[84] The use of the spermicide nonoxynol-9may increase the risk of transmission due to the fact that it causes vaginal and rectal irritation.[85] A vaginal gel containing tenofovir, a reverse transcriptase inhibitor, when used immediately before sex, reduce infection rates by approximately 40% among Africa women.[86]
Circumcision in sub-Saharan Africa reduces the risk of HIV infection in heterosexual men by 38 percent and 66 percent over two years.[87] Based on these studies, the World Health Organizatio and UNAIDS both recommended male circumcision as a method of preventing female-to-male HIV transmission in 2007.[88] Whether it protects against male-to-female transmission is disputed[89][90] and whether it is of benefit in developed countries and among men who have sex with men is undetermined.[91][92][93] Some experts fear that a lower perception of vulnerability among circumcised men may result in more sexual risk-taking behavior, thus negating its preventive effects.[94] Women who have undergone female genital cutting have an increased risk of HIV.[95]
Programs encouraging sexual abstinence do not appear to effect subsequent HIV risk.[96] Evidence for a benefit from peer education is equally poor.[97] Comprehensive sexual education provided at school may decrease high risk behavior.[98] A substantial minority of young people continue to engage in high-risk practices despite HIV/AIDS knowledge, underestimating their own risk of becoming infected with HIV.[99]
Early treatment of HIV-infected people with antiretrovirals protected 96% of partners from infection.[100] Pre-exposure prophylaxis 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, by couples where one is HIV positive, and by young heterosexuals in Africa.[86]
Universal precautions within the health care environment are believed to be effective in decreasing the risk of HIV.[101] Intravenous drug use is an important risk factor and harm reduction strategies such as needle-exchange programmes and opioid substitution therapy appear effective in decreasing this risk.[102]
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.[86] The use of the single agent zidovudine reduces the risk of subsequent HIV infection five fold.[86] Current treatment regimes typical use lopinavir/ritonavir and lamivudine/zidovudine or emtricitabine/tenofovir and may decrease the risk further.[86] The duration of treatment is usually four week[103] and is associated with significant rates of adverse effects (for zidovudine ~70% including: nausea 24%, fatigue 22%, emotional distress 13%, headaches 9%).[50]
Programs to prevent the transmission of HIV from mothers to children can reduce rates of transmission by 92-99%.[102][104] This primarily involves the use of a combination of antivirals during pregnancy and after birth in the infant but also potentially include bottle feeding rather than breastfeeding.[105][104] If replacement feeding is acceptable, feasible, affordable, sustainable and safe mothers should avoid breast-feeding their infants however exclusive breast-feeding is recommended during the first months of life if this is not the case.[106]
As of 2012 there is no effective vaccine for HIV or AIDS.[107] A single trial of the vaccine RV 144 published in 2009 found a partial efficacy rate of ~30% and has stimulated optimism in the research community regarding developing a truly effective vaccine.[108] Further trials of the vaccine are ongoing.[109][110]
There is currently no effective HIV vaccine or cure for HIV/AIDS. Treatment with antiretroviral medications slows progression of the disease[111] and as of 2010 more than 6.6 million people were taking them.[7]
Abacavir – a nucleoside analog reverse transcriptase inhibitor (NARTI or NRTI)
The chemical structure of Abacavir
Current treatment for HIV infection consists of highly active antiretroviral therapy, or HAART which is recommended when CD4 counts are below 350 per microL.[112] Traditionally, treatment has been recommended for people without symptoms when CD4 cell counts fall to 200–250 cells per microliter of blood. However, beginning treatment earlier (at a CD4 level of 350 cells/microliter) may significantly reduce the risk of death.[113] HAART is thought to increase survival time by between 4 and 12 years.[114][115] This has been highly beneficial to many HIV-infected individuals since its introduction in 1996 when the protease inhibitor-based HAART initially became available.[4] Current optimal HAART options consist of combinations (or "cocktails") consisting of at least three drugs belonging to at least two types, or "classes, " of antiretroviral agents.
Typical regimens consist of two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Because HIV disease progression in children is more rapid than in adults, and laboratory parameters are less predictive of risk for disease progression, particularly for young infants, treatment recommendations are more aggressive for children than for adults.[116] In developed countries where HAART is available, the viral load, CD4 counts, rapidity of CD4 decline and patient readiness help determine when to recommend initiating treatment.[117]
Many HIV-infected individuals have experienced improvements in their general health and quality of life, which has led to a decrease of HIV-associated morbidity and mortality.[118][119]
For some people, which can be more than fifty percent, HAART achieves far less than optimal results, due to medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. Non-adherence and non-persistence with therapy are the major reasons why some people do not benefit from HAART.[120] The reasons for non-adherence and non-persistence are varied. Major psychosocial issues include poor access to medical care, inadequate social supports, psychiatric disease and drug abuse. HAART regimens can also be complex and thus hard to follow, with large numbers of pills taken frequently.[121][122][123]
Side effects can also deter people from persisting with HAART, these include lipodystrophy, dyslipidaemia, diarrhoea, insulin resistance, an increase in cardiovascular risks and birth defects.[124] Anti-retroviral drugs are expensive, and the majority of the world's infected individuals do not have access to medications and treatments for HIV and AIDS. However, the costs of anti-retroviral drugs have fallen recently in low-income countries. Moreover, patients' quality of life indices benefit from anti-retroviral treatment especially if healthcare services are adequate.[125] In the absence of a cure for AIDS, anti-retroviral treatment is likely to be a cost-effective strategy for enhancing well-being of AIDS patients and their dependents.
In the US, approximately 60% of people with HIV use various forms of complementary or alternative medicine.[126] The effectiveness of most of these therapies however has not been established.[127] With respect to dietary advice and AIDS some evidence has shown a benefit from micronutrient supplements.[128] Evidence for supplementation with selenium is mixed with some tentative evidence of benefit.[129] There is some evidence that vitamin A supplementation in children reduces mortality and improves growth.[130] In Africa in nutritionally compromised pregnant and lactating women a multivitamin supplementation improved outcomes for both mothers and children.[130] Dietary intake of micronutrients at RDA levels by HIV-infected adults is recommended by the World Health Organization. [131] [132] The WHO further states that several studies indicate that supplementation of vitamin A, zinc, and iron can produce adverse effects in HIV positive adults.[132] In 2005 there was not enough evidence to support the use of herbal medicines.[133]
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
|
1000–2500
2500–5000
5000–7500
7500-10000
10000-50000
≥ 50000
|
Without treatment, the median survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype,[134] and the median survival rate after diagnosis of AIDS in resource-limited settings where treatment is not available ranges between 6 and 19 months.[135] HAART reduces the death rate from this disease by 80%, and raised the life expectancy for a newly diagnosed HIV-infected person to about 20 years.[136]
As new treatments continue to be developed and because HIV continues to evolve resistance to treatments, estimates of survival time are likely to continue to change. Without antiretroviral therapy, death normally occurs within a year after the individual progresses to AIDS.[38] Most patients die from opportunistic infections or malignancies associated with the progressive failure of the immune system.[137] The rate of clinical disease progression varies widely between individuals and has been shown to be affected by many factors such as host susceptibility and immune function[39][40][43] health care and co-infections,[38][137] as well as which particular strain of the virus is involved.[45]
Even with anti-retroviral treatment, over the long term HIV-infected people may experience neurocognitive disorders, osteoporosis, neuropathy, cancers, nephropathy, and cardiovascular disease. It is not always clear whether these conditions result from the infection, related complications, or are side effects of treatment.[138][139][140][29][30][141][124][142]
The largest cause of AIDS morbidity today, globally, is tuberculosis co-infection. In Africa, HIV is the single most important factor contributing to the increase in the incidence of TB since 1990.[143] Life expectancy has fallen in the worst-affected countries; for example, in 2006 it was estimated that it had dropped from 65 to 35 years in Botswana.[5]
Estimated
prevalence of HIV among young adults (15–49) per country at the end of 2005.
HIV infections are considered pandemic by the World Health Organization (WHO).[144] As of 2010 approximately 34 million people have HIV globally.[7] Other these approximately 16.8 million are women and 3.4 million are less than 15 years old.[7] It results in about 1.8 million death in 2010 down from 3.1 million in 2001.[7]
Sub-Saharan Africa is the region most effected. In 2010, an estimated 68% (22.9 million) of all HIV cases and 66% of all deaths (1.2 million) occurred in this region.[145] This means that about 5% of the adult populations is infected.[146] Here in contrast to other regions women compose nearly 60% of cases.[145] South Africa has the largest population of people with HIV of any country in the world at 5.9 million.[145]
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.[146] Approximately 2.4 million of these cases are in India.[145] Prevalence is lowest in Western and Central Europe at 0.2% and East Asia at 0.1%.[146]
In 2008 approximately 1.2 million people have HIV in the United States of which 20% do not realize that they are infected.[147] It resulted in about 17,500 deaths.[147] In the United Kingdom as of 2009 there where approximately 86,500 cases which resulted in 516 deaths.[148] In Canada as of 2008 there where about 65,000 cases which results in 53 deaths.[149] Since AIDS was first recognized in 1981 and 2009 it has led to nearly 30 million deaths.[8]
AIDS was first reported June 5, 1981, when the CDC recorded a cluster of Pneumocystis carinii pneumonia (now still classified as PCP but known to be caused by Pneumocystis jirovecii) in five homosexual men in Los Angeles.[150] In the beginning, 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.[75][76] They also used Kaposi's Sarcoma and Opportunistic Infections, the name by which a task force had been set up in 1981.[151]
In the general press, the term GRID, which stood for gay-related immune deficiency, had been coined.[152] The CDC, in search of a name, and looking at the infected communities coined “the 4H disease, ” as it seemed to single out Haitians, homosexuals, hemophiliacs, and heroin users.[153] However, after determining that AIDS was not isolated to the gay community,[151] the term GRID became misleading and AIDS was introduced at a meeting in July 1982.[154] By September 1982 the CDC started using the name AIDS, and properly defined the illness.[155]
The earliest known positive identification of the HIV-1 virus comes from the Congo in 1959 and 1960 though genetic studies indicate that it passed into the human population from chimpanzees around fifty years earlier.[10] A 2007 study states that a strain of HIV-1 probably moved from Africa to Haiti and then entered the United States around 1969.[156]
HIV descends from the related simian immunodeficiency virus (SIV), which infects apes and monkeys in Africa. There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV.[157] However, only a few of these infections were able to cause epidemics in humans, and all did so in the late 19th—early 20th century. To explain why HIV became epidemic only by that time, there are several theories, each invoking specific driving factors that may have promoted SIV adaptation to humans, or initial spread: social changes following colonialism,[158] rapid transmission of SIV through unsafe or unsterile injections (that is, injections in which the needle is reused without being sterilised),[159] colonial abuses and unsafe smallpox vaccinations or injections,[160] or prostitution and the concomitant high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities.[161][162] See the main article Origin of 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 2 October 1985 having announced that he was suffering from the virus on 25 July that year. It had been diagnosed during 1984.[163] A notable British casualty of AIDS that year was Nicholas Eden, a gay Member of Parliament and son of the late prime minister Anthony Eden.[164][165] The virus claimed perhaps its most famous victim yet on November 24, 1991, when British rock star Freddie Mercury, lead singer of the band Queen, died from an AIDS related illness having only announced that he was suffering from the illness the previous day.[166] However he had been diagnosed as HIV positive during 1987.[167] One of the first high profile heterosexual victims of the virus was Arthur Ashe, the American tennis player. He was diagnosed as HIV positive on 31 August 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.[168] He died, aged 49, as a result of the AIDS virus on 6 February 1993.[169]
A more controversial theory known as the OPV AIDS hypothesis suggests that the AIDS epidemic was inadvertently started in the late 1950s in the Belgian Congo by Hilary Koprowski's research into a poliomyelitis vaccine.[170][171] According to scientific consensus, the available evidence does not support this scenario.[172][173][174]
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.[175] 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.[176]
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.[177]
- Symbolic AIDS stigma—the use of HIV/AIDS to express attitudes toward the social groups or lifestyles perceived to be associated with the disease.[177]
- Courtesy AIDS stigma—stigmatization of people connected to the issue of HIV/AIDS or HIV- positive people.[178]
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.
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 attitudes.[179] There is also a perceived association between AIDS and all male-male sexual behavior, including sex between uninfected men.[177]
Changes in life expectancy in some hard-hit African countries.
Botswana Zimbabwe Kenya South Africa Uganda
HIV and AIDS affects economic growth by reducing the availability of human capital.[180] Without proper nutrition, health care and medicine that is available in developed countries, large numbers of people suffer and die from AIDS-related complications. They will not only be unable to work, but will also require significant medical care. The forecast is that this will probably cause a collapse of economies and societies in countries with a significant AIDS population. In some heavily infected areas, the epidemic has left behind many orphans cared for by elderly grandparents.[181]
The increased mortality has results in a smaller skilled population and labor force. This smaller labor force consists of increasingly younger people, with reduced knowledge and work experience leading to reduced productivity. An increase in workers’ time off to look after sick family members or for sick leave lowers productivity. Increased mortality reduces the mechanisms that generate human capital and investment in people, through loss of income and the death of parents.
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 results in 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.[181]
On the level of the household, AIDS results in both the loss of income and increased spending on healthcare by the household. The income effects of this lead to spending reduction as well as a substitution effect away from education and towards healthcare and funeral spending. A study in Côte d'Ivoire showed that households with an HIV/AIDS patient spent twice as much on medical expenses as other households.[182]
The topic of religion and AIDS has become highly controversial in the past twenty years, primarily because many prominent religious leaders have publicly declared their opposition to the use of condoms,[183][184][Full citation needed] which scientists feel is currently the only means of stopping the epidemic.[citation needed] However, there is a growing openness to faith-based methods due to the failure rates associated with condoms.[184] Other issues involve religious participation in global health care services[citation needed] and collaboration with secular organizations such as UNAIDS and the World Health Organization.[citation needed]
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.[184]
In addition to prevention, some religious groups have interrupted the treatment of AIDS. According to the African Health Policy Network, some churches in London claim that prayer will cure AIDS and the Hackney-based Centre for the Study of Sexual Health and HIV reports that several people have stopped taking their medication, sometimes on the direct advice of their pastor, leading to a number of deaths.[185] The Synagogue Church Of All Nations advertise an "anointing water" to promote God's healing, although the group deny advising people to stop taking medication,[185] and US patent application 2001051133 similarly suggests that intravenous pure distilled water will eradicate HIV through the mercy of God.[186]
Main article:
AIDS denialismA small group of individuals continue to dispute the connection between HIV and AIDS,[187] the existence of HIV itself, or the validity of HIV testing and treatment methods.[188][189] These claims, known as AIDS denialism, have been examined and rejected by the scientific community.[190] However, they have had a significant political impact, particularly in South Africa, where the government's official embrace of AIDS denialism 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.[191][192][193]
Operation INFEKTION was a worldwide Soviet active measures operation to spread information that the United States had created HIV/AIDS. Surveys show that a significant number of people believed – and continue to believe – in such claims.[194]
It has been postulated that only a vaccine can halt the pandemic because a vaccine would possibly cost less, thus being affordable for developing countries, and would not require daily treatments. However, even after almost 30 years of research, HIV-1 remains a difficult target for a vaccine.[195]
Research to improve current treatments includes decreasing side effects of current drugs, further simplifying drug regimens to improve adherence, and determining the best sequence of regimens to manage drug resistance. A number of studies have shown that measures to prevent opportunistic infections can be beneficial when treating patients with HIV infection or AIDS. Vaccination against hepatitis A and B is advised for patients who are not infected with these viruses and are at risk of becoming infected.[196] Patients with substantial immunosuppression are also advised to receive prophylactic therapy for Pneumocystis jiroveci pneumonia (PCP), and many patients may benefit from prophylactic therapy for toxoplasmosis and Cryptococcus meningitis as well.[197]
Researchers have discovered an abzyme that can destroy the protein gp120 CD4 binding site. This protein is common to all HIV variants as it is the attachment point for B lymphocytes and subsequent compromising of the immune system.[198]
Researchers from the Hebrew University of Jerusalem have also discovered that a combination of peptides that stimulate integration together with the protease inhibitor Ro 31-8959 caused apoptotic cell death of HIV-infected cells with total extermination of the virus but did not harm healthy cells.[199][200] It could take several years before a commercial treatment based on this discovery becomes available.[201]
Reactivation of the retrocyclin pseudogene has been proposed as a possible prevention method, as was demonstrated in a proof-of-concept study in tissue culture cells.[202]
In Berlin, Germany, a 42-year-old leukemia patient, Timothy Ray Brown (also referred to as the "Berlin Patient"),[203] infected with HIV for more than a decade was given an experimental transplant of bone marrow with cells that contained an unusual natural variant of the CCR5 cell-surface receptor by a team around Gero Hütter. This CCR5-Δ32 variant has been shown to make some cells from people who are born with it resistant to infection with some strains of HIV. Almost two years after the transplant, and even after the patient reportedly stopped taking antiretroviral medications, HIV has not been detected in the patient's blood.[204] As of December 2010, three years after the transplant, Brown was still free of any detectable HIV in his blood and was described, in a paper in the journal Blood, as "cured".[203][205]
- ^ Sepkowitz KA (June 2001). "AIDS—the first 20 years". N. Engl. J. Med. 344 (23): 1764–72. DOI:10.1056/NEJM200106073442306. PMID 11396444.
- ^ "HIV and Its Transmission". Centers for Disease Control and Prevention. 2003. Archived from the original on February 4, 2005. http://web.archive.org/web/20050204141148/http://www.cdc.gov/HIV/pubs/facts/transmission.htm. Retrieved May 23, 2006.
- ^ "How HIV is spread". San Francisco AIDS Foundation. April 14, 2006. http://www.sfaf.org/aids101/transmission.html. Retrieved May 23, 2006.
- ^ a b Palella FJ Jr, Delaney KM, Moorman AC et al. (1998). "Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators". N. Engl. J. Med. 338 (13): 853–860. DOI:10.1056/NEJM199803263381301. PMID 9516219.
- ^ a b Kallings LO (2008). "The first postmodern pandemic: 25 years of HIV/AIDS". J Intern Med 263 (3): 218–43. DOI:10.1111/j.1365-2796.2007.01910.x. PMID 18205765. http://www.blackwell-synergy.com/doi/full/10.1111/j.1365-2796.2007.01910.x.
- ^ "AIDS epidemic update". World Health Organization. http://www.unaids.org/en/media/unaids/contentassets/dataimport/pub/report/2009/jc1700_epi_update_2009_en.pdf. Retrieved July 29, 2011.
- ^ a b c d e f g UNAIDS 2011 pg. 1-10
- ^ a b "Global Report Fact Sheet". UNAIDS. 2010. http://www.unaids.org/documents/20101123_FS_Global_em_en.pdf.
- ^ Gao F, Bailes E, Robertson DL et al. (1999). "Origin of HIV-1 in the Chimpanzee Pan troglodytes troglodytes". Nature 397 (6718): 436–441. Bibcode 1999Natur.397..436G. DOI:10.1038/17130. PMID 9989410.
- ^ a b Worobey M, Gemmel M, Teuwen DE et al. (October 2008). "Direct evidence of extensive diversity of HIV-1 in Kinshasa by 1960". Nature 455 (7213): 661–4. Bibcode 2008Natur.455..661W. DOI:10.1038/nature07390. PMID 18833279. Archived from the original on March 30 2009. http://www.nature.com/nature/journal/v455/n7213/full/nature07390.html. Retrieved March 31, 2009.
- ^ Gallo RC (2006). "A reflection on HIV/AIDS research after 25 years". Retrovirology 3: 72. DOI:10.1186/1742-4690-3-72. PMC 1629027. PMID 17054781. http://www.retrovirology.com/content/3//72.
- ^ Holmes CB, Losina E, Walensky RP, Yazdanpanah Y, Freedberg KA (2003). "Review of human immunodeficiency virus type 1-related opportunistic infections in sub-Saharan Africa". Clin. Infect. Dis. 36 (5): 656–662. DOI:10.1086/367655. PMID 12594648.
- ^ Guss DA (1994). "The acquired immune deficiency syndrome: an overview for the emergency physician, Part 1". J. Emerg. Med. 12 (3): 375–384. DOI:10.1016/0736-4679(94)90281-X. PMID 8040596.
- ^ Guss DA (1994). "The acquired immune deficiency syndrome: an overview for the emergency physician, Part 2". J. Emerg. Med. 12 (4): 491–497. DOI:10.1016/0736-4679(94)90346-8. PMID 7963396.
- ^ Feldman C (2005). "Pneumonia associated with HIV infection". Curr. Opin. Infect. Dis. 18 (2): 165–170. DOI:10.1097/01.qco.0000160907.79437.5a. PMID 15735422.
- ^ Kwara A, Ramachandran G, Swaminathan S (January 2010). "Dose adjustment of the non-nucleoside reverse transcriptase inhibitors during concurrent rifampicin-containing tuberculosis therapy: one size does not fit all". Expert Opinion on Drug Metabolism & Toxicology 6 (1): 55–68. DOI:10.1517/17425250903393752. PMC 2939445. PMID 19968575. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2939445.
- ^ "Global Tuberculosis Control 2009" (PDF). http://www.who.int/tb/publications/global_report/2009/pdf/full_report.pdf. Retrieved November 1, 2011.
- ^ Decker CF, Lazarus A (August 2000). "Tuberculosis and HIV infection. How to safely treat both disorders concurrently". Postgraduate Medicine 108 (2): 57–60, 65–8. PMID 10951746. http://www.postgradmed.com/index.php?art=pgm_08_2000?article=1181.
- ^ Zaidi SA, Cervia JS (2002). "Diagnosis and management of infectious esophagitis associated with human immunodeficiency virus infection". Journal of the International Association of Physicians in AIDS Care 1 (2): 53–62. DOI:10.1177/154510970200100204. PMID 12942677.
- ^ Pollok RC (2001). "Viruses causing diarrhoea in AIDS". Novartis Foundation Symposium. Novartis Foundation Symposia 238: 276–83; discussion 283–8. DOI:10.1002/0470846534.ch17. ISBN 978-0-470-84653-7. PMID 11444032.
- ^ Guerrant RL, Hughes JM, Lima NL, Crane J (1990). "Diarrhea in developed and developing countries: magnitude, special settings, and etiologies". Reviews of Infectious Diseases 12 (Suppl 1): S41–50. DOI:10.1093/clinids/12.Supplement_1.S41. PMID 2406855.
- ^ Gazzard, B; Balkin, A; Hill, A (2010). "Analysis of neuropsychiatric adverse events during clinical trials of efavirenz in antiretroviral-naive patients: a systematic review". AIDS reviews 12 (2): 67–75. PMID 20571601. edit
- ^ Luft BJ, Chua A (August 2000). "Central Nervous System Toxoplasmosis in HIV Pathogenesis, Diagnosis, and Therapy". Current Infectious Disease Reports 2 (4): 358–362. DOI:10.1007/s11908-000-0016-x. PMID 11095878.
- ^ Sadler M, Nelson MR (June 1997). "Progressive multifocal leukoencephalopathy in HIV". International Journal of STD & AIDS 8 (6): 351–7. DOI:10.1258/0956462971920181. PMID 9179644.
- ^ Gray F, Adle-Biassette H, Chretien F, Lorin de la Grandmaison G, Force G, Keohane C (2001). "Neuropathology and neurodegeneration in human immunodeficiency virus infection. Pathogenesis of HIV-induced lesions of the brain, correlations with HIV-associated disorders and modifications according to treatments". Clinical Neuropathology 20 (4): 146–55. PMID 11495003.
- ^ Grant I, Sacktor H, McArthur J (2005). "HIV neurocognitive disorders". In H.E. Gendelman, I. Grant, I. Everall, S. A. Lipton, and S. Swindells. (ed.) (PDF). The Neurology of AIDS (2nd ed.). London, UK: Oxford University Press. pp. 357–373. ISBN 0-19-852610-5. http://www.hnrc.ucsd.edu/publications_pdf/2005grant1.pdf.
- ^ Satishchandra P, Nalini A, Gourie-Devi M et al. (January 2000). "Profile of neurologic disorders associated with HIV/AIDS from Bangalore, south India (1989–96)". The Indian Journal of Medical Research 111: 14–23. PMID 10793489.
- ^ Wadia RS, Pujari SN, Kothari S et al. (March 2001). "Neurological manifestations of HIV disease". The Journal of the Association of Physicians of India 49: 343–8. PMID 11291974.
- ^ a b Boshoff C, Weiss R (2002). "AIDS-related malignancies". Nat. Rev. Cancer 2 (5): 373–382. DOI:10.1038/nrc797. PMID 12044013.
- ^ a b Yarchoan R, Tosato G, Little RF (2005). "Therapy insight: AIDS-related malignancies – the influence of antiviral therapy on pathogenesis and management". Nat. Clin. Pract. Oncol. 2 (8): 406–415. DOI:10.1038/ncponc0253. PMID 16130937.
- ^ Ho-Yen C and Chang F (June 1, 2008). "Gastrointestinal Malignancies in HIV/AIDS". The AIDS Reader 18 (6). http://www.consultantlive.com/aids/article/1145619/1359079.
- ^ Palefsky J (2007). "Human papillomavirus infection in HIV-infected persons". Top HIV Med 15 (4): 130–3. PMID 17720998.
- ^ Bonnet F, Lewden C, May T et al. (2004). "Malignancy-related causes of death in human immunodeficiency virus-infected patients in the era of highly active antiretroviral therapy". Cancer 101 (2): 317–324. DOI:10.1002/cncr.20354. PMID 15241829.
- ^ Skoulidis, F; Morgan, MS; MacLeod, KM (2004 Aug). "Penicillium marneffei: a pathogen on our doorstep?". Journal of the Royal Society of Medicine 97 (8): 394-6. DOI:10.1258/jrsm.97.8.394. PMC 1079563. PMID 15286196. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1079563.
- ^ Silvero AM, Acevedo-Gadea CR, Pantanowitz L "" (June 4, 2009). "Unsuspected Parvovirus B19 Infection in a Person With AIDS". The AIDS Reader 19 (6). http://www.consultantlive.com/aids/article/1145619/1419436.
- ^ Alimonti JB, Ball TB, Fowke KR (2003). "Mechanisms of CD4+ T lymphocyte cell death in human immunodeficiency virus infection and AIDS". J. Gen. Virol. 84 (7): 1649–1661. DOI:10.1099/vir.0.19110-0. PMID 12810858.
- ^ M. C. I. Lipman, R. W. Baker and M. A. Johnson; with a foreword by P. A. Volberding. (2003). An Atlas of Differential Diagnosis in HIV Disease, Second Edition. CRC Press-Parthenon Publishers. pp. 22–27. ISBN 1-84214-026-4.
- ^ a b c d Morgan D, Mahe C, Mayanja B, Okongo JM, Lubega R, Whitworth JA (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): 597–632. DOI:10.1097/00002030-200203080-00011. PMID 11873003.
- ^ a b Clerici M, Balotta C, Meroni L et al. (1996). "Type 1 cytokine production and low prevalence of viral isolation correlate with long-term non progression in HIV infection". AIDS Res. Hum. Retroviruses. 12 (11): 1053–1061. DOI:10.1089/aid.1996.12.1053. PMID 8827221.
- ^ a b Morgan D, Mahe C, Mayanja B, Whitworth JA (2002). "Progression to symptomatic disease in people infected with HIV-1 in rural Uganda: prospective cohort study". BMJ 324 (7331): 193–196. DOI:10.1136/bmj.324.7331.193. PMC 64788. PMID 11809639. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=64788.
- ^ Gendelman HE, Phelps W, Feigenbaum L et al. (1986). "Transactivation of the human immunodeficiency virus long terminal repeat sequences by DNA viruses". Proc. Natl. Acad. Sci. U.S. A. 83 (24): 9759–9763. Bibcode 1986PNAS...83.9759G. DOI:10.1073/pnas.83.24.9759. PMC 387220. PMID 2432602. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=387220.
- ^ Bentwich Z, Kalinkovich, A, Weisman Z (1995). "Immune activation is a dominant factor in the pathogenesis of African AIDS". Immunol. Today 16 (4): 187–191. DOI:10.1016/0167-5699(95)80119-7. PMID 7734046.
- ^ a b 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): S51–S60. DOI:10.1097/00002030-200317004-00006. PMID 15080180.
- ^ Quiñones-Mateu ME, Mas A, Lain de Lera T, Soriano V, Alcami J, Lederman MM, Domingo E (1998). "LTR and tat variability of HIV-1 isolates from patients with divergent rates of disease progression". Virus Research 57 (1): 11–20. DOI:10.1016/S0168-1702(98)00082-3. PMID 9833881.
- ^ a b Campbell GR, Pasquier E, Watkins J et al. (2004). "The glutamine-rich region of the HIV-1 Tat protein is involved in T-cell apoptosis". J. Biol. Chem. 279 (46): 48197–48204. DOI:10.1074/jbc.M406195200. PMID 15331610.
- ^ Kaleebu P, French N, Mahe C et al. (2002). "Effect of human immunodeficiency virus (HIV) type 1 envelope subtypes A and D on disease progression in a large cohort of HIV-1-positive persons in Uganda". J. Infect. Dis. 185 (9): 1244–1250. DOI:10.1086/340130. PMID 12001041.
- ^ "Facts about AIDS & HIV". avert.org. Archived from the original on December 2 2007. http://www.avert.org/aids.htm. Retrieved November 30, 2007.
- ^ a b Smith, DK; Grohskopf, LA; Black, RJ; Auerbach, JD; Veronese, F; Struble, KA; Cheever, L; Johnson, M; Paxton, LA; Onorato, IM; Greenberg, AE; U.S. Department of Health and Human, Services (2005 Jan 21). "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.
- ^ a b 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.
- ^ a b c d Kripke, C (2007 Aug 1). "Antiretroviral prophylaxis for occupational exposure to HIV.". American family physician 76 (3): 375-6. PMID 17708137.
- ^ a b c d e Dosekun, O; Fox, J (2010 Jul). "An overview of the relative risks of different sexual behaviours on HIV transmission.". Current opinion in HIV and AIDS 5 (4): 291-7. PMID 20543603.
- ^ a b Boily, MC; Baggaley, RF; Wang, L; Masse, B; White, RG; Hayes, RJ; Alary, M (2009 Feb). "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. PMID 19179227.
- ^ Baggaley, RF; White, RG; Boily, MC (2008 Dec). "Systematic review of orogenital HIV-1 transmission probabilities.". International journal of epidemiology 37 (6): 1255-65. PMID 18664564.
- ^ Johnson AM, Laga M (1988). "Heterosexual transmission of HIV". AIDS 2 (suppl. 1): S49–S56. DOI:10.1097/00002030-198800001-00008. PMC 2545554. PMID 3130121. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2545554.
- ^ N'Galy B, Ryder RW (1988). "Epidemiology of HIV infection in Africa". Journal of Acquired Immune Deficiency Syndromes 1 (6): 551–558. PMID 3225742.
- ^ Deschamps MM, Pape JW, Hafner A, Johnson WD Jr. (1996). "Heterosexual transmission of HIV in Haiti". Annals of Internal Medicine 125 (4): 324–330. PMID 8678397.
- ^ Rothenberg RB, Scarlett M, del Rio C, Reznik D, O'Daniels C (1998). "Oral transmission of HIV". AIDS 12 (16): 2095–2105. DOI:10.1097/00002030-199816000-00004. PMID 9833850.
- ^ Mastro TD, de Vincenzi I (1996). "Probabilities of sexual HIV-1 transmission". AIDS 10 (Suppl A): S75–S82. DOI:10.1097/00002030-199601001-00011. PMID 8883613.
- ^ Koenig MA, Zablotska I, Lutalo T, Nalugoda F, Wagman J, Gray R (2004). "Coerced first intercourse and reproductive health among adolescent women in Rakai, Uganda". Int Fam Plan Perspect 30 (4): 156–63. DOI:10.1363/ifpp.30.156.04. PMID 15590381.
- ^ Laga M, Nzila N, Goeman J (1991). "The interrelationship of sexually transmitted diseases and HIV infection: implications for the control of both epidemics in Africa". AIDS 5 (Suppl 1): S55–S63. PMID 1669925.
- ^ Epstein, Helen (2007). The invisible cure: Africa, the West, and the fight against AIDS. New York: Farrar, Straus, and Giroux. ISBN 0-374-28152-1.
- ^ "WHO, UNAIDS Reaffirm HIV as a Sexually Transmitted Disease". WHO. March 17, 2003. http://usinfo.org/wf-archive/2003/030314/epf506.htm. Retrieved January 17, 2006.
- ^ "Financial Resources Required to Achieve, Universal Access to HIV Prevention, Treatment Care and Support" (PDF). UNAIDS. Archived from the original on April 9 2008. http://data.unaids.org/pub/Report/2007/20070925_advocacy_grne2_en.pdf. Retrieved April 11, 2008.
- ^ "Blood safety....for too few". WHO. 2001. http://www.who.int/inf-pr-2000/en/pr2000-25.html. Retrieved January 17, 2006.
- ^ Coovadia HM, Bland RM (2007). "Preserving breastfeeding practice through the HIV pandemic". Trop. Med. Int. Health. 12 (9): 1116–1133. DOI:10.1111/j.1365-3156.2007.01895.x. PMID 17714431.
- ^ Blechner MJ (1997). Hope and mortality: psychodynamic approaches to AIDS and HIV. Hillsdale, NJ: Analytic Press. ISBN 0-88163-223-6.
- ^ Kirby DB, Laris BA, Rolleri LA (March 2007). "Sex and HIV education programs: their impact on sexual behaviors of young people throughout the world". J Adolesc Health 40 (3): 206–17. DOI:10.1016/j.jadohealth.2006.11.143. PMID 17321420.
- ^ Guss DA (1994). "The acquired immune deficiency syndrome: an overview for the emergency physician, Part 1". J Emerg Med 12 (3): 375–84. DOI:10.1016/0736-4679(94)90281-X. PMID 8040596.
- ^ Hel Z, McGhee JR, Mestecky J (June 2006). "HIV infection: first battle decides the war". Trends Immunol. 27 (6): 274–81. DOI:10.1016/j.it.2006.04.007. PMID 16679064.
- ^ 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". J. Exp. Med. 200 (6): 761–70. DOI:10.1084/jem.20041196. PMC 2211967. PMID 15365095. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2211967.
- ^ 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". J. Exp. Med. 200 (6): 749–59. DOI:10.1084/jem.20040874. PMC 2211962. PMID 15365096. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2211962.
- ^ Appay V, Sauce D (January 2008). "Immune activation and inflammation in HIV-1 infection: causes and consequences". J. Pathol. 214 (2): 231–41. DOI:10.1002/path.2276. PMID 18161758.
- ^ 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". Nat. Med. 12 (12): 1365–71. DOI:10.1038/nm1511. PMID 17115046.
- ^ World Health Organization (1990). "Interim proposal for a WHO staging system for HIV infection and disease". WHO Wkly Epidem. Rec. 65 (29): 221–228. PMID 1974812.
- ^ a b Centers for Disease Control (CDC) (1982). "Persistent, generalized lymphadenopathy among homosexual males". MMWR Morb Mortal Wkly Rep. 31 (19): 249–251. PMID 6808340. http://www.cdc.gov/mmwr/preview/mmwrhtml/00001096.htm. Retrieved August 31, 2011.
- ^ a b Barré-Sinoussi F, Chermann JC, Rey F et al. (1983). "Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS)". Science 220 (4599): 868–871. Bibcode 1983Sci...220..868B. DOI:10.1126/science.6189183. PMID 6189183.
- ^ "1993 Revised Classification System for HIV Infection and Expanded Surveillance Case Definition for AIDS Among Adolescents and Adults". CDC. 1992. http://www.cdc.gov/mmwr/preview/mmwrhtml/00018871.htm. Retrieved February 9, 2006.
- ^ a b Kumaranayake L, Watts C (2001). "Resource allocation and priority setting of HIV/AIDS interventions: addressing the generalized epidemic in sub-Saharan Africa". J. Int. Dev. 13 (4): 451–466. DOI:10.1002/jid.798.
- ^ Weber B (2006). "Screening of HIV infection: role of molecular and immunological assays". Expert Rev. Mol. Diagn. 6 (3): 399–411. DOI:10.1586/14737159.6.3.399. PMID 16706742.
- ^ "eMedicine – HIV Infection (Pediatrics: General Medicine)". Medscape.com. http://www.medscape.com/px/trk.svr/emedsearch?exturl=http://emedicine.medscape.com/article/965086-overview. Retrieved November 1, 2011.
- ^ Tóth FD, Bácsi A, Beck Z, Szabó J (2001). "Vertical transmission of human immunodeficiency virus". Acta Microbiol Immunol Hung 48 (3–4): 413–27. DOI:10.1556/AMicr.48.2001.3-4.10. PMID 11791341.
- ^ Crosby, R; Bounse, S (2012 Mar). "Condom effectiveness: where are we now?". Sexual health 9 (1): 10-7. DOI:10.1071/SH11036. PMID 22348628.
- ^ "Condom Facts and Figures". WHO. August 2003. http://www.wpro.who.int/mediacentre/factsheets/fs_200308_Condoms/en/index.html. Retrieved January 17, 2006.
- ^ Gallo, MF; Kilbourne-Brook, M; Coffey, PS (2012 Mar). "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.
- ^ Baptista, M; Ramalho-Santos, J (2009 Nov 1). "Spermicides, microbicides and antiviral agents: recent advances in the development of novel multi-functional compounds.". Mini reviews in medicinal chemistry 9 (13): 1556-67. PMID 20205637.
- ^ a b c d e Celum, C; Baeten, JM (2012 Feb). "Tenofovir-based pre-exposure prophylaxis for HIV prevention: evolving evidence.". Current opinion in infectious diseases 25 (1): 51-7. PMID 22156901.
- ^ Siegfried, N; Muller, M; Deeks, JJ; Volmink, J (2009 Apr 15). "Male circumcision for prevention of heterosexual acquisition of HIV in men.". Cochrane database of systematic reviews (Online) (2): CD003362. PMID 19370585.
- ^ "WHO and UNAIDS announce recommendations from expert consultation on male circumcision for HIV prevention". World Health Organization. Mar 28, 2007. http://www.who.int/mediacentre/news/releases/2007/pr10/en/index.html.
- ^ Larke, N (2010 May 27 – Jun 9). "Male circumcision, HIV and sexually transmitted infections: a review". British journal of nursing (Mark Allen Publishing) 19 (10): 629–34. PMID 20622758.
- ^ Eaton, L; Kalichman, SC (2009 Nov). "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. PMID 19849961.
- ^ Kim, HH; Li, PS, Goldstein, M (2010 Nov). "Male circumcision: Africa and beyond?". Current opinion in urology 20 (6): 515–9. DOI:10.1097/MOU.0b013e32833f1b21. PMID 20844437.
- ^ Templeton, DJ; Millett, GA, Grulich, AE (2010 Feb). "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.
- ^ Wiysonge, CS.; Kongnyuy, EJ.; Shey, M.; Muula, AS.; Navti, OB.; Akl, EA.; Lo, YR. (2011). Wiysonge, Charles Shey. ed. "Male circumcision for prevention of homosexual acquisition of HIV in men". Cochrane Database Syst Rev (6): CD007496. DOI:10.1002/14651858.CD007496.pub2. PMID 21678366.
- ^ Eaton LA, Kalichman S (December 2007). "Risk compensation in HIV prevention: implications for vaccines, microbicides, and other biomedical HIV prevention technologies". Curr HIV/AIDS Rep 4 (4): 165–72. DOI:10.1007/s11904-007-0024-7. PMC 2937204. PMID 18366947. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2937204.
- ^ Utz-Billing I, Kentenich H (December 2008). "Female genital mutilation: an injury, physical and mental harm". J Psychosom Obstet Gynaecol 29 (4): 225–9. DOI:10.1080/01674820802547087. PMID 19065392.
- ^ Underhill K, Operario D, Montgomery P (2008). Operario, Don. ed. "Abstinence-only programs for HIV infection prevention in high-income countries". Cochrane Database of Systematic Reviews (4): CD005421. DOI:10.1002/14651858.CD005421.pub2. PMID 17943855. http://onlinelibrary.wiley.com/o/cochrane/clsysrev/articles/CD005421/frame.html.
- ^ Tolli, MV (2012 May 28). "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. PMID 22641791.
- ^ Ljubojević, S; Lipozenčić, J (2010). "Sexually transmitted infections and adolescence.". Acta dermatovenerologica Croatica : ADC 18 (4): 305-10. PMID 21251451.
- ^ Patel VL, Yoskowitz NA, Kaufman DR, Shortliffe EH (2008). "Discerning patterns of human immunodeficiency virus risk in healthy young adults". Am J Med 121 (4): 758–764. DOI:10.1016/j.amjmed.2008.04.022. PMC 2597652. PMID 18724961. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2597652.
- ^ National Institute of Allergy and Infectious Diseases (NIAID), "Treating HIV-infected People with Antiretrovirals Protects Partners from Infection", NIH News, 2011 May
- ^ Centers for Disease Control (CDC) (August 1987). "Recommendations for prevention of HIV transmission in health-care settings". MMWR 36 (Suppl 2): 1S–18S. PMID 3112554. http://www.cdc.gov/MMWR/PREVIEW/MMWRHTML/00023587.htm.
- ^ a b Kurth, AE; Celum, C; Baeten, JM; Vermund, SH; Wasserheit, JN (2011 Mar). "Combination HIV prevention: significance, challenges, and opportunities.". Current HIV/AIDS reports 8 (1): 62-72. PMID 20941553.
- ^ Young, TN; Arens, FJ; Kennedy, GE; Laurie, JW; Rutherford, G (2007 Jan 24). "Antiretroviral post-exposure prophylaxis (PEP) for occupational HIV exposure.". Cochrane database of systematic reviews (Online) (1): CD002835. DOI:10.1002/14651858.CD002835.pub3. PMID 17253483.
- ^ a b Coutsoudis, A; Kwaan, L; Thomson, M (2010 Oct). "Prevention of vertical transmission of HIV-1 in resource-limited settings.". Expert review of anti-infective therapy 8 (10): 1163-75. PMID 20954881.
- ^ Siegfried, N; van der Merwe, L; Brocklehurst, P; Sint, TT (2011 Jul 6). "Antiretrovirals for reducing the risk of mother-to-child transmission of HIV infection.". Cochrane database of systematic reviews (Online) (7): CD003510. PMID 21735394.
- ^ "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 from the original on April 9 2008. http://www.who.int/hiv/mediacentre/Infantfeedingconsensusstatement.pf.pdf. Retrieved March 12, 2008.
- ^ UNAIDS (May 18th, 2012). "The quest for an HIV vaccine". http://www.unaids.org/en/resources/presscentre/featurestories/2012/may/20120518vaccinesday/.
- ^ Reynell, L; Trkola, A (2012 Mar 2). "HIV vaccines: an attainable goal?". Swiss medical weekly 142: w13535. DOI:10.4414/smw.2012.13535. PMID 22389197.
- ^ U.S. Army Office of the Surgeon General (March 21, 2011). "HIV Vaccine Trial in Thai Adults". ClinicalTrials.gov. http://clinicaltrials.gov/ct2/show/NCT00223080. Retrieved June 28, 2011.
- ^ 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. http://www.clinicaltrials.gov/ct2/show/NCT00337181.
- ^ May, MT; Ingle, SM (2011 Dec). "Life expectancy of HIV-positive adults: a review.". Sexual health 8 (4): 526-33. DOI:10.1071/SH11046. PMID 22127039.
- ^ Vogel, M; Schwarze-Zander, C; Wasmuth, JC; Spengler, U; Sauerbruch, T; Rockstroh, JK (2010 Jul). "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. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2915483.
- ^ Siegfried, N; Uthman, OA; Rutherford, GW (2010 Mar 17). "Optimal time for initiation of antiretroviral therapy in asymptomatic, HIV-infected, treatment-naive adults.". Cochrane database of systematic reviews (Online) (3): CD008272. DOI:10.1002/14651858.CD008272.pub2. PMID 20238364.
- ^ King JT, Justice AC, Roberts MS, Chang CH, Fusco JS and the CHORUS Program Team (2003). "Long-Term HIV/AIDS Survival Estimation in the Highly Active Antiretroviral Therapy Era". Medical Decision Making 23 (1): 9–20. DOI:10.1177/0272989X02239652. PMID 12583451.
- ^ Tassie JM, Grabar S, Lancar R, Deloumeaux J, Bentata M, Costagliola D and the Clinical Epidemiology Group from the French Hospital Database on HIV (2002). "Time to AIDS from 1992 to 1999 in HIV-1-infected subjects with known date of infection". Journal of acquired immune deficiency syndromes 30 (1): 81–7. DOI:10.1097/00126334-200205010-00011. PMID 12048367.
- ^ "Guidelines for the Use of Antiretroviral Agents in Pediatric HIV Infection" (PDF). Department of Health and Human Services Working Group on Antiretroviral Therapy and Medical Management of HIV-Infected Children. November 3, 2005. http://www.aidsinfo.nih.gov/ContentFiles/PediatricGuidelines_PDA.pdf. Retrieved January 17, 2006.
- ^ "Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents" (PDF). Department of Health and Human Services Panel on Clinical Practices for Treatment of HIV Infection. October 6, 2005. http://aidsinfo.nih.gov/ContentFiles/AdultandAdolescentGL.pdf. Retrieved January 17, 2006.
- ^ Palella FJ, Delaney KM, Moorman AC, Loveless MO, Fuhrer J, Satten GA, Aschman DJ, Holmberg SD (1998). "Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection". N. Engl. J. Med. 338 (13): 853–860. DOI:10.1056/NEJM199803263381301. PMID 9516219.
- ^ Chene G, Sterne JA, May M, Costagliola D, Ledergerber B, Phillips AN, Dabis F, Lundgren J, D'Arminio Monforte A, de Wolf F, Hogg R, Reiss P, Justice A, Leport C, Staszewski S, Gill J, Fatkenheuer G, Egger ME and the Antiretroviral Therapy Cohort Collaboration (2003). "Prognostic importance of initial response in HIV-1 infected patients starting potent antiretroviral therapy: analysis of prospective studies". Lancet 362 (9385): 679–686. DOI:10.1016/S0140-6736(03)14229-8. PMID 12957089.
- ^ Becker SL, Dezii CM, Burtcel B, Kawabata H, Hodder S. (2002). "Young HIV-infected adults are at greater risk for medication nonadherence". MedGenMed. 4 (3): 21. PMID 12466764.
- ^ Nieuwkerk P, Sprangers M, Burger D, Hoetelmans RM, Hugen PW, Danner SA, van Der Ende ME, Schneider MM, Schrey G, Meenhorst PL, Sprenger HG, Kauffmann RH, Jambroes M, Chesney MA, de Wolf F, Lange JM and the ATHENA Project (2001). "Limited Patient Adherence to Highly Active Antiretroviral Therapy for HIV-1 Infection in an Observational Cohort Study". Arch. Intern. Med. 161 (16): 1962–1968. DOI:10.1001/archinte.161.16.1962. PMID 11525698.
- ^ Kleeberger C, Phair J, Strathdee S, Detels R, Kingsley L, Jacobson LP (2001). "Determinants of Heterogeneous Adherence to HIV-Antiretroviral Therapies in the Multicenter AIDS Cohort Study". J. Acquir. Immune Defic. Syndr. 26 (1): 82–92. PMID 11176272.
- ^ Heath KV, Singer J, O'Shaughnessy MV, Montaner JS, Hogg RS (2002). "Intentional Nonadherence Due to Adverse Symptoms Associated With Antiretroviral Therapy". J. Acquir. Immune Defic. Syndr. 31 (2): 211–217. DOI:10.1097/00126334-200210010-00012. PMID 12394800.
- ^ a b 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". J. Antimicrob. Chemother. 61 (3): 469–73. DOI:10.1093/jac/dkm499. PMID 18174196. http://jac.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=18174196.
- ^ Bhargava, A.; Booysen, F. L. (2010). "Healthcare infrastructure and emotional support are predictors of CD4 cell counts and quality of life indices of patients on antiretroviral treatment in Free State Province, South Africa". AIDS Care 22 (1): 1–9. DOI:10.1080/09540120903012585. PMID 20390475. edit
- ^ 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. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2570227.
- ^ Mills E, Wu P, Ernst E (June 2005). "Complementary therapies for the treatment of HIV: in search of the evidence". Int J STD AIDS 16 (6): 395–403. DOI:10.1258/0956462054093962. PMID 15969772.
- ^ Irlam, JH; Visser, MM; Rollins, NN; Siegfried, N (2010 Dec 8). "Micronutrient supplementation in children and adults with HIV infection.". Cochrane database of systematic reviews (Online) (12): CD003650. DOI:10.1002/14651858.CD003650.pub3. PMID 21154354.
- ^ Stone, CA; Kawai, K; Kupka, R; Fawzi, WW (2010 Nov). "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. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3066516.
- ^ a b Irlam, JH; Visser, MM; Rollins, NN; Siegfried, N (2010 Dec 8). "Micronutrient supplementation in children and adults with HIV infection.". Cochrane database of systematic reviews (Online) (12): CD003650. DOI:10.1002/14651858.CD003650.pub3. PMID 21154354.
- ^ Forrester, JE; Sztam, KA (2011 Dec). "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. PMID 22089440.
- ^ a b World Health Organization (2003-05). Nutrient requirements for people living with HIV/AIDS: Report of a technical consultation. Geneva. Archived from the original on March 25 2009. http://www.who.int/nutrition/publications/Content_nutrient_requirements.pdf. Retrieved March 31, 2009.
- ^ Liu JP, Manheimer E, Yang M (2005). Liu, Jian Ping. ed. "Herbal medicines for treating HIV infection and AIDS". Cochrane Database Syst Rev (3): CD003937. DOI:10.1002/14651858.CD003937.pub2. PMID 16034917.
- ^ UNAIDS, WHO (December 2007). "2007 AIDS epidemic update" (PDF). http://data.unaids.org/pub/EPISlides/2007/2007_epiupdate_en.pdf. Retrieved March 12, 2008.
- ^ Zwahlen M, Egger M (2006) (PDF). Progression and mortality of untreated HIV-positive individuals living in resource-limited settings: update of literature review and evidence synthesis. UNAIDS Obligation HQ/05/422204. Archived from the original on April 9 2008. http://data.unaids.org/pub/Periodical/2006/zwahlen_unaids_hq_05_422204_2007_en.pdf. Retrieved March 19, 2008.
- ^ Knoll B, Lassmann B, Temesgen Z (2007). "Current status of HIV infection: a review for non-HIV-treating physicians". Int J Dermatol 46 (12): 1219–28. DOI:10.1111/j.1365-4632.2007.03520.x. PMID 18173512.
- ^ a b Lawn SD (2004). "AIDS in Africa: the impact of coinfections on the pathogenesis of HIV-1 infection". J. Infect. Dis. 48 (1): 1–12. DOI:10.1016/j.jinf.2003.09.001. PMID 14667787.
- ^ Woods, S.; Moore, D.; Weber, E.; Grant, I. (2009). "Cognitive neuropsychology of HIV-associated neurocognitive disorders". Neuropsychology review 19 (2): 152–168. DOI:10.1007/s11065-009-9102-5. PMC 2690857. PMID 19462243. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2690857. edit
- ^ Brown, T.; Qaqish, R. (2006). "Antiretroviral therapy and the prevalence of osteopenia and osteoporosis: a meta-analytic review". AIDS (London, England) 20 (17): 2165–2174. DOI:10.1097/QAD.0b013e32801022eb. PMID 17086056. edit
- ^ Nicholas PK, Kemppainen JK, Canaval GE et al. (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.
- ^ Post, F. .; Holt, S. . (2009). "Recent developments in HIV and the kidney". Current opinion in infectious diseases 22 (1): 43–48. DOI:10.1097/QCO.0b013e328320ffec. PMID 19106702. edit
- ^ "AIDS Patients Now Living Longer, But Aging Faster". Npr.org. http://www.npr.org/templates/story/story.php?storyId=120249388. Retrieved November 1, 2011.
- ^ "Tuberculosis". World Health Organization (WHO).
- ^ Tarantola, D. (2000). "Reducing HIV/AIDS risk, impact and vulnerability". Bull World Health Organ vol.78 (no.2). DOI:10.1590/S0042-96862000000200013. ISSN 0042-9686. http://www.scielosp.org/scielo.php?pid=S0042-96862000000200013&script=sci_arttext.
- ^ a b c d UNAIDS 2011 pg. 20-30
- ^ a b c UNAIDS 2011 pg. 40-50
- ^ a b Centers for Disease Control and Prevention, (CDC) (2011 Jun 3). "HIV surveillance--United States, 1981-2008.". MMWR. Morbidity and mortality weekly report 60 (21): 689-93. PMID 21637182.
- ^ Health Protection Agency (2010). HIV in the United Kingdom: 2010 Report. http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1287145367237.
- ^ 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. Ottawa: Public Health Agency of Canada, Centre for Communicable Diseases and Infection Control, Surveillance and Risk Assessment Division. ISBN 978-1-100-52141-1. http://www.phac-aspc.gc.ca/aids-sida/publication/survreport/2009/dec/pdf/2009-Report-Rapport.pdf.
- ^ Gottlieb MS (2006). "Pneumocystis pneumonia—Los Angeles. 1981". Am J Public Health 96 (6): 980–1; discussion 982–3. PMC 1470612. PMID 16714472. Archived from the original on April 22 2009. http://www.cdc.gov/mmwr/preview/mmwrhtml/june_5.htm. Retrieved March 31, 2009.
- ^ a b Centers for Disease Control (CDC) (1982). "Opportunistic infections and Kaposi's sarcoma among Haitians in the United States". MMWR Morb Mortal Wkly Rep. 31 (26): 353–354; 360–361. PMID 6811853. http://www.cdc.gov/mmwr/preview/mmwrhtml/00001123.htm. Retrieved August 31, 2011.
- ^ Altman LK (May 11, 1982). "New homosexual disorder worries health officials". The New York Times. http://www.nytimes.com/1982/05/11/science/new-homosexual-disorder-worries-health-officials.html?scp=1&sq=New%20homosexual%20disorder%20worries%20officials&st=cse. Retrieved August 31, 2011.
- ^ "Making Headway Under Hellacious Circumstances" (PDF). American Association for the Advancement of Science. July 28, 2006. http://www.scienceonline.org/cgi/reprint/313/5786/470b.pdf. Retrieved June 23, 2008.
- ^ Kher U (July 27, 1982). "A Name for the Plague". Time. Archived from the original on March 7 2008. http://www.time.com/time/80days/820727.html. Retrieved March 10, 2008.
- ^ Centers for Disease Control (CDC) (1982). "Update on acquired immune deficiency syndrome (AIDS)—United States". MMWR Morb Mortal Wkly Rep. 31 (37): 507–508; 513–514. PMID 6815471.
- ^ Gilbert MT, Rambaut A, Wlasiuk G, Spira TJ, Pitchenik AE, Worobey M (2007). "The emergence of HIV/AIDS in the Americas and beyond". Proc. Natl. Acad. Sci. U.S. A. 104 (47): 18566–70. Bibcode 2007PNAS..10418566G. DOI:10.1073/pnas.0705329104. PMC 2141817. PMID 17978186. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2141817.
- ^ Kalish ML, Wolfe ND, Ndongmo CD, McNicholl J, Robbins KE et al. (2005). "Central African hunters exposed to simian immunodeficiency virus". Emerg Infect Dis 11 (12): 1928–30. DOI:10.3201/eid1112.050394. PMID 16485481.
- ^ Sharp, P. M.; Bailes, E.; Chaudhuri, R. R.; Rodenburg, C. M.; Santiago, M. O.; Hahn, B. H. (2001). "The origins of acquired immune deficiency syndrome viruses: where and when?". Philosophical Transactions of the Royal Society B: Biological Sciences 356 (1410): 867–76. DOI:10.1098/rstb.2001.0863. PMC 1088480. PMID 11405934. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1088480.
- ^ Marx PA, Alcabes PG, Drucker E (2001). "Serial human passage of simian immunodeficiency virus by unsterile injections and the emergence of epidemic human immunodeficiency virus in Africa". Philos Trans R Soc Lond B Biol Sci 356 (1410): 911–20. DOI:10.1098/rstb.2001.0867. PMC 1088484. PMID 11405938. http://rstb.royalsocietypublishing.org/content/356/1410/911.abstract.
- ^ Chitnis, Amit; Rawls, Diana; Moore, Jim (2000). "Origin of HIV Type 1 in Colonial French Equatorial Africa?". AIDS Research and Human Retroviruses 16 (1): 5–8. DOI:10.1089/088922200309548. PMID 10628811.
- ^ Sousa, João Dinis de; Müller, Viktor; Lemey, Philippe; Vandamme, Anne-Mieke; Vandamme, Anne-Mieke (2010). Martin, Darren P.. ed. "High GUD Incidence in the Early 20th Century Created a Particularly Permissive Time Window for the Origin and Initial Spread of Epidemic HIV Strains". PLoS ONE 5 (4): e9936. DOI:10.1371/journal.pone.0009936. PMC 2848574. PMID 20376191. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2848574.
- ^ Donald G. McNeil, Jr. (September 16, 2010). "Precursor to H. I. V. Was in Monkeys for Millennia". New York Times. Archived from the original on September 19 2010. http://www.nytimes.com/2010/09/17/health/17aids.html?_r=1&src=me&ref=general. Retrieved September 17, 2010. "Dr. Marx believes that the crucial event was the introduction into Africa of millions of inexpensive, mass-produced syringes in the 1950s. ... suspect that the growth of colonial cities is to blame. Before 1910, no Central African town had more than 10,000 people. But urban migration rose, increasing sexual contacts and leading to red-light districts."
- ^ "Rock Hudson announces he has AIDS – History.com This Day in History – 7/25/1985". History.com. http://www.history.com/this-day-in-history/rock-hudson-announces-he-has-aids. Retrieved November 1, 2011.
- ^ "Anthony Eden". Nndb.com. http://www.nndb.com/people/817/000088553/. Retrieved November 1, 2011.
- ^ Coleman, Brian (June 25, 2007). "Thatcher the gay icon". New Statesman. http://www.newstatesman.com/blogs/brian-coleman/2007/06/lady-thatcher-gay-tory. Retrieved November 1, 2011.
- ^ "BBC ON THIS DAY | 24 | 1991: Giant of rock dies". BBC News. November 24, 1963. http://news.bbc.co.uk/onthisday/hi/dates/stories/november/24/newsid_2546000/2546945.stm. Retrieved November 1, 2011.
- ^ "Freddie Mercury". Nndb.com. http://www.nndb.com/people/521/000044389/. Retrieved November 1, 2011.
- ^ http://www.itennisstore.com/Tennis-Latest-News/FROZEN-IN-TIME—ARTHUR-ASHE-by-Dominic-Bliss.aspx
- ^ The Independent (London). February 8, 1993. http://www.independent.co.uk/news/tributes-to-arthur-ashe-1471622.html.
- ^ Curtis T (1992). "The origin of AIDS". Rolling Stone (626): pp. 54–59, 61, 106, 108. Archived from the original on February 17, 2008. http://web.archive.org/web/20080217014508/http://www.uow.edu.au/arts/sts/bmartin/dissent/documents/AIDS/Curtis92.html. Retrieved March 10, 2008.
- ^ Hooper E (1999). The River: A Journey to the Source of HIV and AIDS (1st ed.). Boston, Massachusetts: Little Brown & Co. pp. 1–1070. ISBN 0-316-37261-7.
- ^ Worobey M, Santiago ML, Keele BF et al. (2004). "Origin of AIDS: contaminated polio vaccine theory refuted". Nature 428 (6985): 820. Bibcode 2004Natur.428..820W. DOI:10.1038/428820a. PMID 15103367.
- ^ Berry N, Jenkins A, Martin J et al. (2005). "Mitochondrial DNA and retroviral RNA analyses of archival oral polio vaccine (OPV CHAT) materials: evidence of macaque nuclear sequences confirms substrate identity". Vaccine 23 (14): 1639–1648. DOI:10.1016/j.vaccine.2004.10.038. PMID 15705467.
- ^ "Oral Polio Vaccine and HIV / AIDS: Questions and Answers". Centers for Disease Control and Prevention. March 23, 2004. http://www.cdc.gov/nip/vacsafe/concerns/aids/poliovac-hiv-aids-qa.htm. Retrieved November 20, 2006.
- ^ "The impact of AIDS on people and societies" (PDF). 2006 Report on the global AIDS epidemic. UNAIDS. 2006. ISBN 92-9173-479-9. http://data.unaids.org/pub/GlobalReport/2006/2006_GR_CH04_en.pdf. Retrieved June 14, 2006.
- ^ Ogden J, Nyblade L (2005). "Common at its core: HIV-related stigma across contexts" (PDF). International Center for Research on Women. http://www.icrw.org/docs/2005_report_stigma_synthesis.pdf. Retrieved February 15, 2007.
- ^ a b c Herek GM, Capitanio JP (1999). "AIDS Stigma and sexual prejudice" (PDF). American Behavioral Scientist 42 (7): 1130–1147. DOI:10.1177/0002764299042007006. http://psychology.ucdavis.edu/rainbow/html/abs99_sp.pdf. Retrieved March 27, 2006.
- ^ Snyder M, Omoto AM, Crain AL (1999). "Punished for their good deeds: stigmatization for AIDS volunteers". American Behavioral Scientist 42 (7): 1175–1192. DOI:10.1177/0002764299042007009.
- ^ Herek GM, Capitanio JP, Widaman KF (2002). "HIV-related stigma and knowledge in the United States: prevalence and trends, 1991–1999" (PDF). Am J Public Health 92 (3): 371–7. DOI:10.2105/AJPH.92.3.371. PMC 1447082. PMID 11867313. Archived from the original on March 7 2008. http://psychology.ucdavis.edu/rainbow/html/ajph2002.pdf. Retrieved March 10, 2008.
- ^ Bell C, Devarajan S, Gersbach H (2003) (PDF). org/hiv_aids/docs/BeDeGe_BP_total2.pdf The long-run economic costs of AIDS: theory and an application to South Africa. World Bank Policy Research Working Paper No. 3152. http://www1.worldbank. org/hiv_aids/docs/BeDeGe_BP_total2.pdf. Retrieved April 28, 2008.
- ^ a b Greener R (2002). "AIDS and macroeconomic impact". In S, Forsyth (ed.). State of The Art: AIDS and Economics. IAEN. pp. 49–55.
- ^ Over M (1992) (PDF). The macroeconomic impact of AIDS in Sub-Saharan Africa, Population and Human Resources Department. The World Bank. Archived from the original on May 27 2008. http://www.worldbank.org/aidsecon/macro.pdf. Retrieved May 3, 2008.
- ^ "AIDS Stigma". News-medical.net. http://www.news-medical.net/health/AIDS-Stigma.aspx. Retrieved November 1, 2011.
- ^ a b c "Thirty years after AIDS discovery, appreciation growing for Catholic approach". Catholicnewsagency.com. June 5, 2011. http://www.catholicnewsagency.com/news/thirty-years-after-aids-discovery-appreciation-growing-for-catholic-approach/?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+catholicnewsagency%2Fdailynews+%28CNA+Daily+News%29. Retrieved November 1, 2011.
- ^ a b "Church HIV prayer cure claims 'cause three deaths'". BBC News. October 18, 2011. http://www.bbc.co.uk/news/uk-england-london-14406818. Retrieved October 18, 2011.
- ^ US application 2001051133
- ^ Duesberg, P. H. (1988). "HIV is not the cause of AIDS". Science 241 (4865): 514, 517. Bibcode 1988Sci...241..514D. DOI:10.1126/science.3399880. PMID 3399880. Cohen, J. (1994). "The Controversy over HIV and AIDS" (PDF). Science 266 (5191): 1642–1649. Bibcode 1994Sci...266.1642C. DOI:10.1126/science.7992043. PMID 7992043. http://www.sciencemag.org/feature/data/cohen/266-5191-1642a.pdf. Retrieved 2009-03-31.
- ^ Kalichman, Seth (2009). Denying AIDS: Conspiracy Theories, Pseudoscience, and Human Tragedy. New York: Copernicus Books (Springer Science+Business Media). ISBN 978-0-387-79475-4. http://books.google.com/?id=_mtDBCDwxugC&printsec=frontcover&q=.
- ^ Smith TC, Novella SP (August 2007). "HIV Denial in the Internet Era". PLoS Med. 4 (8): e256. DOI:10.1371/journal.pmed.0040256. PMC 1949841. PMID 17713982. http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0040256&ct=1&SESSID=3d4baa1a64e57d8ff33e9d41eb2335a1. Retrieved 2009-11-07.
- ^
- ^ Watson J (2006). "Scientists, activists sue South Africa's AIDS 'denialists'". Nat. Med. 12 (1): 6. DOI:10.1038/nm0106-6a. PMID 16397537.
- ^ Baleta A (2003). "S Africa's AIDS activists accuse government of murder". Lancet 361 (9363): 1105. DOI:10.1016/S0140-6736(03)12909-1. PMID 12672319.
- ^ Cohen J (2000). "South Africa's new enemy". Science 288 (5474): 2168–70. DOI:10.1126/science.288.5474.2168. PMID 10896606.
- ^ Operation INFEKTION – Soviet Bloc Intelligence and Its AIDS Disinformation Campaign. Thomas Boghardt. 2009
- ^ Karlsson Hedestam GB, Fouchier RA, Phogat S, Burton DR, Sodroski J, Wyatt RT (February 2008). "The challenges of eliciting neutralizing antibodies to HIV-1 and to influenza virus". Nat. Rev. Microbiol. 6 (2): 143–55. DOI:10.1038/nrmicro1819. PMID 18197170.
- ^ Laurence J (2006). "Hepatitis A and B virus immunization in HIV-infected persons". AIDS Reader 16 (1): 15–17. PMID 16433468.
- ^ "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. http://www.guideline.gov/summary/summary.aspx?ss=14&doc_id=6223&string=infected+AND+patients. Retrieved February 5, 2007.
- ^ Planque S, Nishiyama Y, Taguchi H, Salas M, Hanson C, Paul S (June 2008). "Catalytic antibodies to HIV: Physiological role and potential clinical utility". Autoimmun Rev 7 (6): 473–9. DOI:10.1016/j.autrev.2008.04.002. PMC 2527403. PMID 18558365. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2527403.
- ^ Even, Dan (September 3, 2010). "Hebrew U. researchers develop treatment to kill HIV cells". Haaretz. Archived from the original on September 6 2010. http://www.haaretz.com/print-edition/news/hebrew-u-researchers-develop-treatment-to-kill-hiv-cells-1.311823. Retrieved October 11, 2010.
- ^ Levin, Aviad; Hayouka, Zvi; Friedler, Assaf; Loyter; Abraham (August 19, 2010). "Specific eradication of HIV-1 from infected cultured cells". AIDS Research and Therapy 7 (31): 31. DOI:10.1186/1742-6405-7-31. PMC 2933580. PMID 20723214. Archived from the original on August 26 2010. http://www.aidsrestherapy.com/content/7/1/31. Retrieved October 11, 2010.
- ^ Klein Leichman, Abigail (October 7, 2010). org/201010038374/health/on-the-hiv-warpath "On the HIV warpath". Israel 21c Innovation News Service. http://israel21c. org/201010038374/health/on-the-hiv-warpath. Retrieved October 11, 2010.
- ^ "Retrocyclin pseudogene reactivation as defense to AIDS". Plosbiology.org. http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1000095. Retrieved November 1, 2011.
- ^ a b "German HIV patient cured after stem cell transplant". Belfast Telegraph. December 15, 2010. http://www.belfasttelegraph.co.uk/news/world-news/german-hiv-patient-cured-after-stem-cell-transplant-15030473.html. Retrieved December 15, 2010.
- ^ Schoofs, Mark (November 2008). "A Doctor, a Mutation and a Potential Cure for AIDS: A Bone Marrow Transplant to Treat a Leukemia Patient Also Gives Him Virus-Resistant Cells; Many Thanks, Sample 61". Wall Street Journal. http://online.wsj.com/article/SB122602394113507555.html. Retrieved November 12, 2008.
- ^ Allers, K.; Hutter, G.; Hofmann, J.; Loddenkemper, C.; Rieger, K.; Thiel, E.; Schneider, T. (2010). "Evidence for the cure of HIV infection by CCR5 32/ 32 stem cell transplantation". Blood 117 (10): 2791–2799. DOI:10.1182/blood-2010-09-309591. PMID 21148083. edit
- References
This audio file was created from a revision of the "
AIDS" article dated 2012-04-10, and does not reflect subsequent edits to the article. (
Audio help)
|
|
|
| HIV |
|
|
| Conditions |
|
|
| History |
|
|
| Social |
|
|
| Culture |
|
|
|
|
|
|
|
|
|
lez:КъИДС
_300mg.jpg)
