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Human immunodeficiency virus (HIV) is a lentivirus (a member of the retrovirus family) that causes acquired immunodeficiency syndrome (AIDS),[1][2] a condition in humans in which the immune system begins to fail, leading to life-threatening opportunistic infections. 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 white blood cells. The four major routes of transmission are unsafe sex, contaminated needles, breast milk, and transmission from an infected mother to her baby at birth (vertical transmission). 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 considered pandemic by the World Health Organization (WHO). Nevertheless, complacency about HIV may play a key role in HIV risk.[3][4] From its discovery in 1981 to 2006, AIDS killed more than 25 million people.[5] HIV infects about 0.6% of the world's population.[5] In 2005 alone, AIDS claimed an estimated 2.4–3.3 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.[6] According to current estimates, HIV is set to infect 90 million people in Africa, resulting in a minimum estimate of 18 million orphans.[7] Antiretroviral treatment reduces both the mortality rate and the morbidity of HIV infection, but routine access to antiretroviral medication is not available in all countries.[8]

HIV infects primarily vital cells in the human immune system such as helper T cells (to be specific, CD4+ T cells), macrophages, and dendritic cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: First, direct viral killing of infected cells; second, increased rates of apoptosis in infected cells; and third, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections.

Most untreated people infected with HIV-1 eventually develop AIDS. These individuals mostly die from opportunistic infections or malignancies associated with the progressive failure of the immune system.[9] HIV progresses to AIDS at a variable rate affected by viral, host, and environmental factors; most will progress to AIDS within 10 years of HIV infection: some will have progressed much sooner, and some will take much longer.[10][11] Treatment with anti-retrovirals increases the life expectancy of people infected with HIV. Even after HIV has progressed to diagnosable AIDS, the average survival time with antiretroviral therapy was estimated to be more than 5 years as of 2005.[12] Without antiretroviral therapy, someone who has AIDS typically dies within a year.[13]

ReferencesEdit

  1. Weiss RA (May 1993). "How does HIV cause AIDS?". Science 260 (5112): 1273–9. PMID 8493571. 
  2. Douek DC, Roederer M, Koup RA (2009). "Emerging concepts in the immunopathogenesis of AIDS". Annu. Rev. Med. 60: 471–84. doi:10.1146/annurev.med.60.041807.123549. PMID 18947296. 
  3. http://www.cdc.gov/hiv/resources/reports/hiv_prev_us.htm
  4. http://www.cdc.gov/nchhstp/newsroom/docs/FastFacts-MSM-FINAL508COMP.pdf
  5. 5.0 5.1 Joint United Nations Programme on HIV/AIDS (2006). "Overview of the global AIDS epidemic", 2006 Report on the global AIDS epidemic (PDF). Retrieved on 2006-06-08. 
  6. Greener, R. (2002). "AIDS and macroeconomic impact", in S, Forsyth (ed.): State of The Art: AIDS and Economics. IAEN, 49–55. 
  7. Joint United Nations Programme on HIV/AIDS. AIDS epidemic update, 2005 (PDF). Retrieved on 2006-02-28.
  8. 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. (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. 
  9. 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. 
  10. Buchbinder SP, Katz MH, Hessol NA, O'Malley PM, Holmberg SD. (1994). "Long-term HIV-1 infection without immunologic progression". AIDS 8 (8): 1123–8. doi:10.1097/00002030-199408000-00014. PMID 7986410. 
  11. "Time from HIV-1 seroconversion to AIDS and death before widespread use of highly active antiretroviral therapy: a collaborative re-analysis. Collaborative Group on AIDS Incubation and HIV Survival including the CASCADE EU Concerted Action. Concerted Action on SeroConversion to AIDS and Death in Europe" (April 2000). Lancet 355 (9210): 1131–7. doi:10.1016/S0140-6736(00)02061-4. PMID 10791375. 
  12. Schneider MF, Gange SJ, Williams CM, Anastos K, Greenblatt RM, Kingsley L, Detels R, Munoz A (2005). "Patterns of the hazard of death after AIDS through the evolution of antiretroviral therapy: 1984–2004". AIDS 19 (17): 2009–18. PMID 16260908. 
  13. 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. PMID 11873003. 

External linksEdit


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