Abstract:
Cell activation is probably required for conversion of a latent HIV infection into an active one. Herpes simplex virus (HSV) may provide the appropriate antigenic stimulus, as discussed here. HSV infections (type 1, HSV-1 and type 2, HSV-2) are widely distributed and do not appear to be restricted by race, age, or socioeconomic group. Prevalence rates are 90-100% in persons at high risk for AIDS. Of potential interest for AIDS pathogenesis is the propensity of HSV to establish latent (nonproductive) infection with subsequent episodes of virus reactivation. The widely held view that HSV reactivation results in clinical symptoms has been challenged recently by accumulating evidence of subclinical virus reactivation. Cell-mediated immunity is widely accepted as playing a role in HSV infection. However, its exact contribution to latency and recurrent disease is not clear. Differences in the magnitude of HSV-specific blastogenic response and natural killer cell activity of mononuclear cells from patients (pts) with recurrent disease (compared to seropositive controls) have been seen in some studies but not others. The concept that HSV-induced immunosuppression may contribute to AIDS pathogenesis agrees with recent findings indicating that many immunologic abnormalities detected in pts with AIDS are due to CD4+ T-cell dysfunction rather than HIV-induced cytolysis. Mononuclear cells from 0/5 pts with AIDS, 3/5 pts with AIDS-related complex (ARC), and 3/5 homosexual controls failed to produce lymphokines in response to HSV-2 antigen. Addition of interleukin-1 (IL-1) restored this function to the cells from all pts with ARC and all the controls, but not to those from the pts with AIDS. These findings suggest that HSV- and HIV-immunosuppressive effects are additive and/or synergistic. Both HIV and HSV infect monocytes/macrophages and Ia+ epidermal cells in which direct HIV activation can take place. Also, macrophage infection with either virus causes functional alterations, including failure to produce IL-1, generation of prostaglandin E, and the induction of suppressor T-cell (Ts) circuitries. If HSV is involved in HIV activation, preventive anti-HSV therapy may be helpful. Herpesviruses, particularly HSV, can augment HIV expression by direct recognition of sequences within the HIV promoter. Ts-cell induction and suppressor-factor production are a natural aspect of the pathogenesis of HSV infection and contribute to the immune dysfunction that characterizes AIDS. (35 Refs)
Keywords: Herpes Simplex/*IMMUNOLOGY/PREVENTION & CONTROL Human HIV/*IMMUNOLOGY HIV Infections/*IMMUNOLOGY Immunity, Cellular/PHYSIOLOGY Lymphokines/PHYSIOLOGY Opportunistic Infections/*IMMUNOLOGY/PREVENTION & CONTROL Recurrence Risk Factors Simplexvirus/IMMUNOLOGY Virus Activation/IMMUNOLOGY JOURNAL ARTICLE REVIEW REVIEW, TUTORIAL 900530
M9051002
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