Abstract

HIV infection affects various parts of the immune system, including the CD4+ lymphocytes and mononuclear phagocytes, and causes a progressive immunodeficiency. This renders the patient susceptible to various opportunistic infections and neoplasms. Reactive oxygen intermediates (ROI) are important for the intracellular killing of microorganisms by mononuclear phagocytes and neutrophils. Although data are discrepant, several studies suggest that the generation of ROI is impaired in mononuclear phagocytes, and possibly also in neutrophils, from HIV-infected individuals. This may lead to deficient killing of intracellular microorganisms predisposing the HIV-infected patient to certain opportunistic infections. Recently, in vitro studies have shown that ROI activate the intracellular transcription factor nuclear factor kappa B (NF-kappa B) which stimulates HIV replication. Intracellular antioxidant systems, such as the glutathione system, seem to be of importance for the regulation of ROI levels and thus probably for HIV replication in vitro. However, the role of ROI in regulation of HIV replication in vivo is unknown at present. The role of ROI in HIV infection is thus difficult to assess, both at the cellular and clinical level. Reduced intracellular concentrations of ROI may lead to impaired phagocyte microbicidal functions, thus predisposing HIV-infected patients to various opportunistic infections. On the other hand, increased ROI levels may be associated with a stimulation of HIV replication leading to clinical deterioration.