3rd International AIDS Conference Washington, DC, U.S.A. — June 1-5, 1987

Int Conf AIDS. 1987 Jun 1-5;3:1 Abstract No. M.2.3

Peter Piot
Institute of Tropical Medicine, Antwerp, Belgium

The clinical expression of HIV-infection appears increasingly complex. It includes manifestations due to opportunistic diseases, as well as illness directly caused by HIV itself. Neurological disease may include involvement of brain, spinal cord and peripheral nerves, and is probably directly caused by HIV, as is lymphocytic interstitial pneumonia. The etiology of chronic diarrhea and a papular pruritic skin eruption associated with HIV-infection is unclear. Several clinical classification systems for HIV-infection have been proposed. Between 2 and 8 % of infected individuals per year progress to AIDS, with no apparent decrease in the rate of disease progression over time. Within 5 to 10 years of infection the majority of infected persons develop clinical disease. Reported risk factors and/or predictors of disease progression such as a decreased number of T-helper lymphocytes, an increased number of T-suppressor lymphocytes, a low level of HIV-antibody and a high titer of CMV-antibody, may be markers or reflect duration of infection. A chronically activated state secondary to chronic viral and parasitic antigenic exposure may increase both the susceptibility to HIV-infection and development of disease. Increased HIV gene expression and persistent antigenemia may also be contributing factors in disease development. Persistent viral production in monocyte/macrophage cells in the brain and elsewhere may be a source of virus production in other organs. Infection of the brain implies that HIV may be protected from immune surveillance or therapeutic intervention.

870601
M.2.3

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