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WHO Disease Staging System for HIV Infection and Disease in Adults and Adolescents information


WHO Disease Staging System for HIV Infection and Disease in Adults and Adolescents was first produced in 1990 by the World Health Organization[1] and updated in September 2005. It is an approach for use in resource limited settings and is widely used in Africa and Asia and has been a useful research tool in studies of progression to symptomatic HIV disease.[2]

Following infection with HIV, the rate of clinical disease progression varies enormously between individuals. Many factors such as host susceptibility and immune function,[2][3][4] health care and co-infections,[5][6][7] as well as factors relating to the viral strain [8][9] may affect the rate of clinical disease progression.

  1. ^ WHO; Mahe, C; Mayanja, B; Whitworth, JA (1990). "Interim proposal for a WHO Staging System for HIV infection and Disease" (PDF). Wkly Epidemiol Rec. 65 (29): 221–224. PMID 1974812.
  2. ^ 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.
  3. ^ Clerici M, Balotta C, Meroni L, Ferrario E, Riva C, Trabattoni D, Ridolfo A, Villa M, Shearer GM, Moroni M, Galli M (1996). "Type 1 cytokine production and low prevalence of viral isolation correlate with long-term nonprogression in HIV infection". AIDS Res Hum Retroviruses. 12 (11): 1053–1061. doi:10.1089/aid.1996.12.1053. PMID 8827221.
  4. ^ 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.
  5. ^ Gendelman HE, Phelps W, Feigenbaum L, Ostrove JM, Adachi A, Howley PM, Khoury G, Ginsberg HS, Martin MA (1986). "Trans-activation of the human immunodeficiency virus long terminal repeat sequence 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.
  6. ^ 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.
  7. ^ 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): 597–603. doi:10.1097/00002030-200203080-00011. PMID 11873003. S2CID 35450422.
  8. ^ Quinones-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 Res. 57 (1): 11–20. doi:10.1016/S0168-1702(98)00082-3. PMID 9833881.
  9. ^ Campbell GR, Pasquier E, Watkins J, Bourgarel-Rey V, Peyrot V, Esquieu D, Barbier P, de Mareuil J, Braguer D, Kaleebu P, Yirrell DL, Loret EP (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.

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