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