Human Immunodeficiency Virus (HIV): Difference between revisions

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==Classification==
==Classification==
HIV is a member of the genus [[Lentivirus]],<ref name=ICTV61.0.6>{{cite web
| author=[[International Committee on Taxonomy of Viruses]]
| publisher=[[National Institutes of Health]]
| publishyear=2002
| url=http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/61060000.htm
| title=61.0.6. Lentivirus
| accessdate=2006-02-28
}}</ref> part of the family of [[Retroviridae]].<ref name=ICTV61.>{{cite web
| author=[[International Committee on Taxonomy of Viruses]]
| publisher=[[National Institutes of Health]]
| publishyear=2002
| url=http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/61000000.htm
| title=61. Retroviridae
| accessdate=2006-02-28
}}</ref> 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.<ref name=Levy>{{cite journal
| author=Lévy, J. A.
| title=HIV pathogenesis and long-term survival
| journal=AIDS
| year=1993
| pages=1401-1410
| volume=7
| issue=11
| pmid=8280406
| format=
}}</ref> Lentiviruses are transmitted as single-stranded, positive-[[Sense (molecular biology)|sense]], enveloped [[RNA virus]]es. 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 [[Transcription (genetics)|transcribed]]. Once the virus has infected the cell, two pathways are possible: either the virus becomes [[Incubation period|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.<ref name=Gao>{{cite journal
| author=Gao, F., Bailes, E., Robertson, D. L., Chen, Y., Rodenburg, C. M., Michael, S. F., Cummins, L. B., Arthur, L. O., Peeters, M., Shaw, G. M., Sharp, P. M., and Hahn, B. H.
| title=Origin of HIV-1 in the Chimpanzee Pan troglodytes troglodytes
| journal=Nature
| year=1999
| pages=436-441
| volume=397
| issue=6718
| pmid=9989410
| doi=10.1038/17130
| format=
}}</ref><ref name=Keele>{{cite journal
| author=Keele, B. F., van Heuverswyn, F., Li, Y. Y., Bailes, E., Takehisa, J., Santiago, M. L., Bibollet-Ruche, F., Chen, Y., Wain, L. V., Liegois, F., Loul, S., Mpoudi Ngole, E., Bienvenue, Y., Delaporte, E., Brookfield, J. F. Y., Sharp, P. M., Shaw, G. M., Peeters, M., and Hahn, B. H.
| title=Chimpanzee Reservoirs of Pandemic and Nonpandemic HIV-1
| journal=Science | year=2006 | pages= | volume=Online [[2006-05-25]] | issue=
| url= http://www.sciencemag.org/cgi/content/abstract/1126531
| doi = 10.1126/science.1126531
| format=
}}</ref> 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.<ref name=Reeves>{{cite journal
| author=Reeves, J. D. and Doms, R. W
| title=Human Immunodeficiency Virus Type 2
| journal=J. Gen. Virol. | year=2002 | pages=1253-1265 | volume=83 | issue=Pt 6
| pmid=12029140
}}</ref> HIV-2 is less transmittable than HIV-1 and is largely confined to West Africa.<ref name=Reeves>{{cite journal
| author=Reeves, J. D. and Doms, R. W
| title=Human Immunodeficiency Virus Type 2
| journal=J. Gen. Virol. | year=2002 | pages=1253-1265 | volume=83 | issue=Pt 6
| pmid=12029140
}}</ref>


==Early history==
==Early history==

Revision as of 21:03, 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

Early history

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

Transmission

Structure and genome

Tropism

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.[1] 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.[2] 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.[3] 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. [4]

History and physical findings for primary HIV infection[4]
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.[5] 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.[6]

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

Treatment

Epidemiology

AIDS denialism

Main article: AIDS reappraisal

A small minority of scientists and activists question the connection between HIV and AIDS,[7] the existence of HIV itself,[8] or the validity of current testing and treatment methods. These claims have been examined and widely rejected by the scientific community,[9] 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.[10][11][12]

Related Chapters

References

  1. ↑ Piatak, M., Jr, Saag, M. S., Yang, L. C., Clark, S. J., Kappes, J. C., Luk, K. C., Hahn, B. H., Shaw, G. M. and Lifson, J.D. (1993). "High levels of HIV-1 in plasma during all stages of infection determined by competitive PCR". Science. 259 (5102): 1749–1754. doi:10.1126/science.8096089. PMID 8096089.
  2. ↑ Pantaleo G, Demarest JF, Schacker T, Vaccarezza M, Cohen OJ, Daucher M, Graziosi C, Schnittman SS, Quinn TC, Shaw GM, Perrin L, Tambussi G, Lazzarin A, Sekaly RP, Soudeyns H, Corey L, Fauci AS. (1997). "The qualitative nature of the primary immune response to HIV infection is a prognosticator of disease progression independent of the initial level of plasma viremia". Proc Natl Acad Sci U S A. 94 (1): 254–258. PMID 8990195.
  3. ↑ Kahn, J. O. and Walker, B. D. (1998). "Acute Human Immunodeficiency Virus type 1 infection". N. Engl. J. Med. 331 (1): 33–39. PMID 9647878.
  4. ↑ 4.0 4.1 Daar ES, Little S, Pitt J; et al. (2001). "Diagnosis of primary HIV-1 infection. Los Angeles County Primary HIV Infection Recruitment Network". Ann. Intern. Med. 134 (1): 25–9. PMID 11187417.
  5. ↑ Burton GF, Keele BF, Estes JD, Thacker TC, Gartner S. (2002). "Follicular dendritic cell contributions to HIV pathogenesis". Semin Immunol. 14 (4): 275–284. PMID 12163303.
  6. ↑ Clapham PR, McKnight A. (2001). "HIV-1 receptors and cell tropism". Br Med Bull. 58 (4): 43–59. PMID 11714623.
  7. ↑ Duesberg, P. H. (1988). "HIV is not the cause of AIDS". Science. 241 (4865): 514, 517. doi:10.1126/science.3399880. PMID 3399880.
  8. ↑ Papadopulos-Eleopulos, E., Turner, V. F., Papadimitriou, J., Page, B., Causer, D., Alfonso, H., Mhlongo, S., Miller, T., Maniotis, A. and Fiala, C. (2004). "A critique of the Montagnier evidence for the HIV/AIDS hypothesis". Med Hypotheses. 63 (4): 597&ndash, 601. PMID 15325002.
  9. ↑ For evidence of the scientific consensus that HIV is the cause of AIDS, see (for example):
  10. ↑ Watson J (2006). "Scientists, activists sue South Africa's AIDS 'denialists'". Nat. Med. 12 (1): 6. doi:10.1038/nm0106-6a. PMID 16397537.
  11. ↑ 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.
  12. ↑ Cohen J (2000). "South Africa's new enemy". Science. 288 (5474): 2168–70. doi:10.1126/science.288.5474.2168. PMID 10896606.

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