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

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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.

Revised World Health Organization (WHO) Clinical Staging of HIV/AIDS For Adults and Adolescents (2005)[edit]

(This is the interim African Region version for persons aged 15 years or more who have had a positive HIV antibody test or other laboratory evidence of HIV infection) (The United Nations defines adolescents as persons aged 10−19 years but for surveillance purposes, the category of adults and adolescents comprises people aged 15 years and over)

Primary HIV infection[edit]

Clinical stage 1[edit]

Clinical stage 2[edit]

Clinical stage 3[edit]

Conditions where a presumptive diagnosis can be made on the basis of clinical signs or simple investigations

  • Unexplained chronic diarrhoea for longer than one month
  • Unexplained persistent fever (intermittent or constant for longer than one month)
  • Severe weight loss (>10% of presumed or measured body weight)
  • Oral candidiasis
  • Oral hairy leukoplakia
  • Pulmonary tuberculosis (TB) diagnosed in last two years
  • Severe presumed bacterial infections (e.g. pneumonia, empyema, meningitis, bacteraemia, pyomyositis, bone or joint infection)
  • Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis

Conditions where confirmatory diagnostic testing is necessary

  • Unexplained anaemia (< 80 g/l), and or neutropenia (<500/µl) and or thrombocytopenia (<50 000/ µl) for more than one month

Clinical stage 4[edit]

Conditions where a presumptive diagnosis can be made on the basis of clinical signs or simple investigations

Conditions where confirmatory diagnostic testing is necessary

Original proposal in 1990[edit]

Clinical Stage I[edit]

  • Asymptomatic
  • Generalised lymphadenopathy
  • In some cases symptoms similar to those of cold flue would be manifested.

Performance scale: 1: asymptomatic, normal activity.

Clinical Stage II[edit]

  • Weight loss, < 10% of body weight
  • Minor mucocutaneous manifestations (seborrheic dermatitis, prurigo, fungal nail infections, recurrent oral ulcerations, angular cheilitis)
  • Herpes zoster within the last five years
  • Recurrent upper respiratory tract infections (i.e. bacterial sinusitis)

And/or performance scale 2: symptomatic, normal activity.

Clinical Stage III[edit]

And/or performance scale 3: bedridden < 50% of the day during last month.

Clinical Stage IV[edit]

The declaration of AIDS

And/or performance scale 4: bedridden > 50% of the day during last month.

(*) HIV wasting syndrome: weight loss of > 10% of body weight, plus either unexplained chronic diarrhoea (> 1 month) or chronic weakness and unexplained prolonged fever (> 1 month).

(**) HIV encephalopathy: clinical findings of disabling cognitive and/or motor dysfunction interfering with activities of daily living, progressing over weeks to months, in the absence of a concurrent illness or condition other than HIV infection which could explain the findings.


  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. PMC 64788Freely accessible. PMID 11809639. doi:10.1136/bmj.324.7331.193. 
  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. PMID 8827221. doi:10.1089/aid.1996.12.1053. 
  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. PMID 15080180. doi:10.1097/00002030-200317004-00006. 
  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. PMC 387220Freely accessible. PMID 2432602. doi:10.1073/pnas.83.24.9759. 
  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. PMID 7734046. doi:10.1016/0167-5699(95)80119-7. 
  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. PMID 11873003. doi:10.1097/00002030-200203080-00011. 
  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. PMID 9833881. doi:10.1016/S0168-1702(98)00082-3. 
  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. PMID 15331610. doi:10.1074/jbc.M406195200.