Human Immunodeficiency Virus (HIV): Difference between revisions

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{{HIV}}  
{{HIV}}  
==Overview==
==Overview==
'''Human immunodeficiency virus''' ('''HIV''') is a [[retrovirus]] that can lead to ''[[acquired immunodeficiency syndrome]]'' (AIDS), a condition in [[human]]s in which the [[immune system]] begins to fail, leading to life-threatening opportunistic infections. Previous names for the [[virus]] include '''human T-lymphotropic virus-III''' ('''HTLV-III'''), '''lymphadenopathy-associated virus''' ('''LAV'''), and '''AIDS-associated retrovirus''' ('''ARV''').<ref>{{cite web| author=Rick Sowadsky| year=1999 |url=http://thebody.org/Forums/AIDS/safesex/Archive/origins/Q8777.html |title=What is HTLV-III?| accessdate=2006-08-24}}</ref><ref name=Coffin>{{cite journal
| author=Coffin, J., Haase, A., Levy, J. A., Montagnier, L., Oroszlan, S., Teich, N., Temin, H., Toyoshima, K., Varmus, H., Vogt, P. and Weiss, R. A. | title=What to call the AIDS virus? | journal=Nature | year=1986 | pages=10 | volume=321 | issue=6065 | pmid=3010128 |format=}}</ref>
Infection with HIV occurs by the transfer of [[blood]], [[semen]], [[vaginal fluid]], [[pre-ejaculate]], or [[breast milk]]. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells. The four major routes of transmission are [[unprotected sex|unprotected sexual intercourse]], contaminated needles, breast milk, and transmission from an infected mother to her baby at [[childbirth|birth]]. Screening of blood products for HIV has largely eliminated transmission through blood transfusions or infected blood products in the developed world.
HIV infection in humans is now [[pandemic]]. As of January 2006, the [[Joint United Nations Programme on HIV/AIDS]] (UNAIDS) and the [[World Health Organization]] (WHO) estimate that AIDS has killed more than 25 million people since it was first recognized on December 1, 1981, making it one of the most destructive [[AIDS pandemic|pandemics]] in recorded history.  It is estimated that about 0.6% of the world's population is infected with HIV.<ref name=UNAIDS2006>{{cite book
| author =[[Joint United Nations Programme on HIV/AIDS]]
| year = 2006
| title = 2006 Report on the global AIDS epidemic
| chapter = Overview of the global AIDS epidemic
| chapterurl = http://data.unaids.org/pub/GlobalReport/2006/2006_GR_CH02_en.pdf
| accessdate = 2006-06-08
| format= [[PDF|PDF format]]
}}</ref> In 2005 alone, AIDS claimed an estimated 2.4&ndash;3.3 million lives, of which more than 570,000 were children. A third of these deaths are occurring in sub-Saharan Africa, retarding economic growth and increasing poverty.<ref name=Greener>{{cite book
| author =Greener, R.
| year = 2002
| title = State of The Art: AIDS and Economics
| chapter = AIDS and macroeconomic impact
| chapterurl = http://www.iaen.org/library/statepidemic/chapter7.pdf
| editor = S, Forsyth (ed.)
| edition =
| pages = 49-55
| publisher = IAEN
| format= PDF
| location =
}}</ref> According to current estimates, HIV is set to infect 90 million people in Africa, resulting in a minimum estimate of 18 million orphans.<ref name=UNAIDS>{{cite web
| author=[[Joint United Nations Programme on HIV/AIDS]]
| publisher=
| publishyear= 2005
| url=http://www.unaids.org/Epi2005/doc/EPIupdate2005_pdf_en/epi-update2005_en.pdf
| title=AIDS epidemic update, 2005
| accessdate=2006-02-28|format=[[PDF|PDF format]]
}}</ref> [[antiretroviral drug|Antiretroviral]] treatment reduces both the [[Mortality rate|mortality]] and the [[morbidity]] of HIV infection, but routine access to antiretroviral medication is not available in all countries.<ref name=Palella>{{cite journal
| author=Palella, F. J. Jr, Delaney, K. M., Moorman, A. C., Loveless, M. O., Fuhrer, J., Satten, G. A., Aschman and D. J., Holmberg, S. D.
| title=Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators
| journal=N. Engl. J. Med
| year=1998
| pages=853-860
| volume=338
| issue=13
| pmid=9516219
| format=
}}</ref>
HIV primarily infects vital cells in the [[human]] [[immune system]] such as [[helper T cell]]s (specifically CD4<SUP>+</SUP> T cells), [[macrophages]] and [[dendritic cells]]. HIV infection leads to low levels of CD4<SUP>+</SUP> T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of [[apoptosis]] in infected cells; and thirdly, killing of infected CD4<SUP>+</SUP> T cells by [[CD8 cytotoxic lymphocyte]]s that recognize infected cells. When CD4<SUP>+</SUP> T cell numbers decline below a critical level, [[cell-mediated immunity]] is lost, and the body becomes progressively more susceptible to opportunistic infections. If untreated, eventually most HIV-infected individuals develop [[AIDS|AIDS (Acquired Immunodeficiency Syndrome)]] and die; however about one in ten remains healthy for many years, with no noticeable symptoms.<ref name=Buchbinder>{{cite journal
| author=Buchbinder SP, Katz MH, Hessol NA, O'Malley PM, Holmberg SD.
| title=Long-term HIV-1 infection without immunologic progression.
| journal=AIDS
| year=1994
| pages=1123-1128
| volume=8
| issue=8
| pmid=7986410
| format=
}}</ref> Treatment with anti-retrovirals, where available, increases the life expectancy of people infected with HIV. It is hoped that current and future treatments may allow HIV-infected individuals to achieve a life expectancy approaching that of the general public.


==Origin and discovery==
==Origin and discovery==

Revision as of 19:54, 23 April 2012

Template:DiseaseDisorder infobox

Human immunodeficiency virus
Stylized rendering of a cross section of the human immunodeficiency virus
Stylized rendering of a cross section
of the human immunodeficiency virus
Virus classification
Group: Group VI (ssRNA-RT)
Family: Retroviridae
Genus: Lentivirus
Species
  • Human immunodeficiency virus 1
  • Human immunodeficiency virus 2

To read more about AIDS, click here.

To read about the difference between HIV & AIDS, click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Template:HIV

Overview

Origin and discovery

See AIDS origin

Classification

HIV is a member of the genus Lentivirus,[1] part of the family of Retroviridae.[2] Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period.[3] Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genome is converted to double-stranded DNA by a virally encoded reverse transcriptase that is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integrase so that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latent and the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.

Two species of HIV infect humans: HIV-1 and HIV-2. HIV-1 is thought to have originated in southern Cameroon after jumping from wild chimpanzees (Pan troglodytes troglodytes) to humans during the twentieth century.[4][5] HIV-1 is the virus that was initially discovered and termed LAV. It is more virulent and relatively easy transmitted and is the cause of the majority of HIV infections globally. HIV-2 may have originated from the Sooty Mangabey (Cercocebus atys), an Old World monkey of Guinea-Bissau, Gabon, and Cameroon.[6] HIV-2 is less transmittable than HIV-1 and is largely confined to West Africa.[6]

Early history

See History of known cases and spread for early cases of HIV / AIDS

Transmission

Structure and genome

Tropism

The term viral tropism refers to which cell types HIV infects. HIV can infect a variety of immune cells such as CD4+ T cells, macrophages, and microglial cells. HIV-1 entry to macrophages and CD4+ T cells is mediated through interaction of the virion envelope glycoproteins (gp120) with the CD4 molecule on the target cells and also with chemokine coreceptors.[7]

Macrophage (M-tropic) strains of HIV-1, or non-syncitia-inducing strains (NSI) use the β-chemokine receptor CCR5 for entry and are thus able to replicate in macrophages and CD4+ T cells.[8] This CCR5 coreceptor is used by almost all primary HIV-1 isolates regardless of viral genetic subtype. Indeed, macrophages play a key role in several critical aspects of HIV infection. They appear to be the first cells infected by HIV and perhaps the source of HIV production when CD4+ cells become depleted in the patient. Macrophages and microglial cells are the cells infected by HIV in the central nervous system. In tonsils and adenoids of HIV-infected patients, macrophages fuse into multinucleated giant cells that produce huge amounts of virus.

T-tropic isolates, or syncitia-inducing (SI) strains replicate in primary CD4+ T cells as well as in macrophages and use the α-chemokine receptor, CXCR4, for entry.[8][9][10] Dual-tropic HIV-1 strains are thought to be transitional strains of the HIV-1 virus and thus are able to use both CCR5 and CXCR4 as co-receptors for viral entry.

The α-chemokine, SDF-1, a ligand for CXCR4, suppresses replication of T-tropic HIV-1 isolates. It does this by down-regulating the expression of CXCR4 on the surface of these cells. HIV that use only the CCR5 receptor are termed R5, those that only use CXCR4 are termed X4, and those that use both, X4R5. However, the use of coreceptor alone does not explain viral tropism, as not all R5 viruses are able to use CCR5 on macrophages for a productive infection[8] and HIV can also infect a subtype of myeloid dendritic cells,[11] which probably constitute a reservoir that maintains infection when CD4+ T cell numbers have declined to extremely low levels.

Some people are resistant to certain strains of HIV.[12] One example of how this occurs is people with the CCR5-Δ32 mutation; these people are resistant to infection with R5 virus as the mutation stops HIV from binding to this coreceptor, reducing its ability to infect target cells.

Sexual intercourse is the major mode of HIV transmission. Both X4 and R5 HIV are present in the seminal fluid which is passed from partner to partner. The virions can then infect numerous cellular targets and disseminate into the whole organism. However, a selection process leads to a predominant transmission of the R5 virus through this pathway.[13][14][15] How this selective process works is still under investigation, but one model is that spermatozoa may selectively carry R5 HIV as they possess both CCR3 and CCR5 but not CXCR4 on their surface[16] and that genital epithelial cells preferentially sequester X4 virus.[17] In patients infected with subtype B HIV-1, there is often a co-receptor switch in late-stage disease and T-tropic variants appear that can infect a variety of T cells through CXCR4.[18] These variants then replicate more aggressively with heightened virulence that causes rapid T cell depletion, immune system collapse, and opportunistic infections that mark the advent of AIDS.[19] Thus, during the course of infection, viral adaptation to the use of CXCR4 instead of CCR5 may be a key step in the progression to AIDS. A number of studies with subtype B-infected individuals have determined that between 40 and 50% of AIDS patients can harbour viruses of the SI, and presumably the X4, phenotype.[20][21]

Replication cycle

Genetic variability

The clinical course of infection

For more details on this topic, see AIDS Diagnosis, AIDS Symptoms and Complications and WHO Disease Staging System for HIV Infection and Disease
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. Template:Legend-line Template:Legend-line

Infection with HIV-1 is associated with a progressive decrease of the CD4+ T cell count and an increase in viral load. The stage of infection can be determined by measuring the patient's CD4+ T cell count, and the level of HIV in the blood.

The initial infection with HIV generally occurs after transfer of body fluids from an infected person to an uninfected one. The first stage of infection, the primary, or acute infection, is a period of rapid viral replication that immediately follows the individual's exposure to HIV leading to an abundance of virus in the peripheral blood with levels of HIV commonly approaching several million viruses per mL.[22] This response is accompanied by a marked drop in the numbers of circulating CD4+ T cells. This acute viremia is associated in virtually all patients with the activation of CD8+ T cells, which kill HIV-infected cells, and subsequently with antibody production, or seroconversion. The CD8+ T cell response is thought to be important in controlling virus levels, which peak and then decline, as the CD4+ T cell counts rebound to around 800 cells per mL (the normal value is 1200 cells per mL ). A good CD8+ T cell response has been linked to slower disease progression and a better prognosis, though it does not eliminate the virus.[23] During this period (usually 2-4 weeks post-exposure) most individuals (80 to 90%) develop an influenza or mononucleosis-like illness called acute HIV infection, the most common symptoms of which may include fever, lymphadenopathy, pharyngitis, rash, myalgia, malaise, mouth and esophagal sores, and may also include, but less commonly, headache, nausea and vomiting, enlarged liver/spleen, weight loss, thrush, and neurological symptoms. Infected individuals may experience all, some, or none of these symptoms. The duration of symptoms varies, averaging 28 days and usually lasting at least a week.[24] Because of the nonspecific nature of these symptoms, they are often not recognized as signs of HIV infection. Even if patients go to their doctors or a hospital, they will often be misdiagnosed as having one of the more common infectious diseases with the same symptoms. Consequently, these primary symptoms are not used to diagnose HIV infection as they do not develop in all cases and because many are caused by other more common diseases. However, recognizing the syndrome can be important because the patient is much more infectious during this period. [25]

History and physical findings for primary HIV infection[25]
sensitivity specificity
Fever 88% 50%
Malaise 73% 58%
Myalgia 60% 74%
Rash 58% 79%
Headache 55% 56%
Night sweats 50% 68%
Sore throat 43% 51%
Lymphadenopathy 38% 71%
Arthralgia 28% 87%
Nasal congestion 18% 62%

A strong immune defense reduces the number of viral particles in the blood stream, marking the start of the infection's clinical latency stage. Clinical latency can vary between two weeks and 20 years. During this early phase of infection, HIV is active within lymphoid organs, where large amounts of virus become trapped in the follicular dendritic cells (FDC) network.[26] The surrounding tissues that are rich in CD4+ T cells may also become infected, and viral particles accumulate both in infected cells and as free virus. Individuals who are in this phase are still infectious. During this time, CD4+ CD45RO+ T cells carry most of the proviral load.[27]

When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and infections with a variety of opportunistic microbes appear. The first symptoms often include moderate and unexplained weight loss, recurring respiratory tract infections (such as sinusitis, bronchitis, otitis media, pharyngitis), prostatitis, skin rashes, and oral ulcerations. Common opportunistic infections and tumors, most of which are normally controlled by robust CD4+ T cell-mediated immunity then start to affect the patient. Typically, resistance is lost early on to oral Candida species and to Mycobacterium tuberculosis, which leads to an increased susceptibility to oral candidiasis (thrush) and tuberculosis. Later, reactivation of latent herpes viruses may cause worsening recurrences of herpes simplex eruptions, shingles, Epstein-Barr virus-induced B-cell lymphomas, or Kaposi's sarcoma, a tumor of endothelial cells that occurs when HIV proteins such as Tat interact with Human Herpesvirus-8. Pneumonia caused by the fungus Pneumocystis jirovecii is common and often fatal. In the final stages of AIDS, infection with cytomegalovirus (another herpes virus) or Mycobacterium avium complex is more prominent. Not all patients with AIDS get all these infections or tumors, and there are other tumors and infections that are less prominent but still significant.

HIV test

Main article: HIV test

Many HIV-positive people are unaware that they are infected with the virus.[28] For example, less than 1% of the sexually active urban population in Africa have been tested and this proportion is even lower in rural populations.[28] Furthermore, only 0.5% of pregnant women attending urban health facilities are counselled, tested or receive their test results.[28] Again, this proportion is even lower in rural health facilities.[28] Since donors may therefore be unaware of their infection, donor blood and blood products used in medicine and medical research are routinely screened for HIV.

HIV-1 testing consists of initial screening with an enzyme-linked immunosorbent assay (ELISA) to detect antibodies to HIV-1. Specimens with a nonreactive result from the initial ELISA are considered HIV-negative unless new exposure to an infected partner or partner of unknown HIV status has occurred. Specimens with a reactive ELISA result are retested in duplicate.[29] If the result of either duplicate test is reactive, the specimen is reported as repeatedly reactive and undergoes confirmatory testing with a more specific supplemental test (e.g., Western blot or, less commonly, an immunofluorescence assay (IFA)). Only specimens that are repeatedly reactive by ELISA and positive by IFA or reactive by Western blot are considered HIV-positive and indicative of HIV infection. Specimens that are repeatedly ELISA-reactive occasionally provide an indeterminate Western blot result, which may be either an incomplete antibody response to HIV in an infected person, or nonspecific reactions in an uninfected person.[30] Although IFA can be used to confirm infection in these ambiguous cases, this assay is not widely used. Generally, a second specimen should be collected more than a month later and retested for persons with indeterminate Western blot results. Although much less commonly available, nucleic acid testing (e.g., viral RNA or proviral DNA amplification method) can also help diagnosis in certain situations.[29] In addition, a few tested specimens might provide inconclusive results because of a low quantity specimen. In these situations, a second specimen is collected and tested for HIV infection.

Treatment

See also AIDS Treatment and Antiretroviral drug.
Abacavir - a nucleoside analog reverse transcriptase inhibitors (NARTIs or NRTIs)
The chemical structure of Abacavir

There is currently no vaccine or cure for HIV or AIDS. The only known method of prevention is avoiding exposure to the virus. However, an antiretroviral treatment, known as post-exposure prophylaxis, is believed to reduce the risk of infection if begun directly after exposure.[31] Current treatment for HIV infection consists of highly active antiretroviral therapy, or HAART.[32] This has been highly beneficial to many HIV-infected individuals since its introduction in 1996, when the protease inhibitor-based HAART initially became available.[33] Current HAART options are combinations (or "cocktails") consisting of at least three drugs belonging to at least two types, or "classes," of anti-retroviral agents. Typically, these classes are two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Because AIDS progression in children is more rapid and less predictable than in adults, particularly in young infants, more aggressive treatment is recommended for children than adults.[34] In developed countries where HAART is available, doctors assess their patients thoroughly: measuring the viral load, how fast CD4 declines, and patient readiness. They then decide when to recommend starting treatment.[35]

HAART allows the stabilisation of the patient’s symptoms and viremia, but it neither cures the patient, nor alleviates the symptoms; high levels of HIV-1, often HAART resistant, return once treatment is stopped.[36][37] Moreover, it would take more than a lifetime for HIV infection to be cleared using HAART.[38] Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to a large reduction in HIV-associated morbidity and mortality in the developed world.[33][39][40] A computer based study in 2006 projected that following the 2004 United States treatment guidelines gave an average life expectancy of an HIV infected individual to be 32.1 years from the time of infection if treatment was started when the CD4 count was 350/µL.[41] This study was limited as it did not take into account possible future treatments and the projection has not been confirmed within a clinical cohort setting. In the absence of HAART, progression from HIV infection to AIDS has been observed to occur at a median of between nine to ten years and the median survival time after developing AIDS is only 9.2 months.[42] However, HAART sometimes achieves far less than optimal results, in some circumstances being effective in less than fifty percent of patients. This is due to a variety of reasons such as medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. However, non-adherence and non-persistence with antiretroviral therapy is the major reason most individuals fail to benefit from HAART.[43] The reasons for non-adherence and non-persistence with HAART are varied and overlapping. Major psychosocial issues, such as poor access to medical care, inadequate social supports, psychiatric disease and drug abuse contribute to non-adherence. The complexity of these HAART regimens, whether due to pill number, dosing frequency, meal restrictions or other issues along with side effects that create intentional non-adherence also contribute to this problem.[44][45][46] The side effects include lipodystrophy, dyslipidaemia, insulin resistance, an increase in cardiovascular risks and birth defects.[47][48]

The timing for starting HIV treatment is still debated. There is no question that treatment should be started before the patient's CD4 count falls below 200, and most national guidelines say to start treatment once the CD4 count falls below 350; but there is some evidence from cohort studies that treatment should be started before the CD4 count falls below 350.[49][39] There is also evidence to say that treatment should be started before CD4 percentage falls below 15%.[50] In those countries where CD4 counts are not available, patients with WHO stage III or IV disease[51] should be offered treatment.

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.[52] 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. Unfortunately, only a vaccine is thought to be able to halt the pandemic. This is because a vaccine would cost less, thus being affordable for developing countries, and would not require daily treatment.[52] However, after over 20 years of research, HIV-1 remains a difficult target for a vaccine.[52] In February 2007, The National Institute of Allergy and Infectious Diseases published a report that gave details of a region on HIV's surface that is a potential target for a vaccine.[53]

Researchers at the Heinrich Pette Institute of Experimental Virology and Immunology at Hamburg have engineered an enzyme called Cre recombinase which is able to remove HIV from an infected cell.[54] Similarly, scientists at the Max Planck Institute for Molecular Cell Biology and Genetics in Dresden have engineered an enzyme called Tre recombinase which is able to remove HIV from an infected cell.[55] These enzymes promise a treatment in which a patient's stem cells are extracted, cured, and reinjected to promulgate the enzyme into the body. The carried enzyme then finds and removes the virus.

Epidemiology

Main article: AIDS pandemic
Prevalence of HIV among adults per country at the end of 2005
  15–50%
  5–15%
  1–5%
  0.5–1.0%
  0.1–0.5%
  <0.1%
  no data

UNAIDS and the WHO estimate that AIDS has killed more than 25 million people since it was first recognized in 1981, making it one of the most destructive pandemics in recorded history. Despite recent improved access to antiretroviral treatment and care in many regions of the world, the AIDS pandemic claimed an estimated 2.8 million (between 2.4 and 3.3 million) lives in 2005 of which more than half a million (570,000) were children.[56]

Globally, between 33.4 and 46 million people currently live with HIV.[56] In 2005, between 3.4 and 6.2 million people were newly infected and between 2.4 and 3.3 million people with AIDS died, an increase from 2004 and the highest number since 1981.

Sub-Saharan Africa remains by far the worst-affected region, with an estimated 21.6 to 27.4 million people currently living with HIV. Two million [1.5–3.0 million] of them are children younger than 15 years of age. More than 64% of all people living with HIV are in sub-Saharan Africa, as are more than three quarters of all women living with HIV. In 2005, there were 12.0 million [10.6–13.6 million] AIDS orphans living in sub-Saharan Africa 2005.[56] South & South East Asia are second-worst affected with 15% of the total. AIDS accounts for the deaths of 500,000 children in this region. South Africa has the largest number of HIV patients in the world followed by Nigeria.[57] India has an estimated 2.5  million infections (0.23% of population), making India the country with the third largest population of HIV patients. In the 35 African nations with the highest prevalence, average life expectancy is 48.3 years—6.5 years less than it would be without the disease.[58]

The latest evaluation report of the World Bank's Operations Evaluation Department assesses the development effectiveness of the World Bank's country-level HIV/AIDS assistance defined as policy dialogue, analytic work, and lending with the explicit objective of reducing the scope or impact of the AIDS epidemic.[59] This is the first comprehensive evaluation of the World Bank's HIV/AIDS support to countries, from the beginning of the epidemic through mid-2004. Because the Bank aims to assist in implementation of national government programmes, their experience provides important insights on how national AIDS programmes can be made more effective.

The development of HAART as effective therapy for HIV infection and AIDS has substantially reduced the death rate from this disease in those areas where these drugs are widely available. This has created the misperception that the disease has vanished. In fact, as the life expectancy of persons with AIDS has increased in countries where HAART is widely used, the number of persons living with AIDS has increased substantially. In the United States, the number of persons with AIDS increased from about 35,000 in 1988 to over 220,000 in 1996.[60]

In Africa, the number of MTCT and the prevalence of AIDS is beginning to reverse decades of steady progress in child survival. Countries such as Uganda are attempting to curb the MTCT epidemic by offering VCT (voluntary counselling and testing), PMTCT (prevention of mother-to-child transmission) and ANC (ante-natal care) services, which include the distribution of antiretroviral therapy.

AIDS denialism

Main article: AIDS reappraisal

A small minority of scientists and activists question the connection between HIV and AIDS,[61] the existence of HIV itself,[62] or the validity of current testing and treatment methods. These claims have been examined and widely rejected by the scientific community,[63] although they have had a political impact, particularly in South Africa, where governmental acceptance of AIDS denialism has been blamed for an ineffective response to that country's AIDS epidemic.[64][65][66]

Related Chapters

References

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  2. ↑ International Committee on Taxonomy of Viruses. "61. Retroviridae". National Institutes of Health. Retrieved 2006-02-28. Unknown parameter |publishyear= ignored (help)
  3. ↑ Lévy, J. A. (1993). "HIV pathogenesis and long-term survival". AIDS. 7 (11): 1401–1410. PMID 8280406.
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