The reservoirs of HIV-1 infection that permit maintenance of persistent virus infection (even when virus replication cannot be detected using sensitive assays to quantify plasma HIV-1 RNA levels) are currently unknown. Potential sites for persistent HIV-1 infection include cells with chronic or latent infections, cells present in locations within the body where antiviral drugs may not penetrate in levels sufficient to prevent additional cycles of de novo virus infection (e.g., the central nervous system), the presence of susceptible target cells for virus infection that may not metabolize certain antiviral drugs to their active inhibitory forms (e.g., macrophages), or extracellular (possible infectious) virus that may be retained on the surface of follicular dendritic cells within lymphoid organs. In an attempt to determine which, if any, of these potential reservoirs contribute to persistent HIV-1 infection, HIV-1-infected persons in two groups categorized by CD4+ T cell levels will be treated with concomitant administration of 4 antiviral drugs (zidovudine, lamivudine, indinavir and nevirapine) to accomplish maximal achievable suppression of virus replication. The rates of decay of virus and virus-infected cells following initiation of antiviral (and steroid) therapy will be monitored with sensitive, quantitative assays, and the identity and longevity of persistent sites of infection will be determined. This study may also illuminate to what extent HIV-1-induced immune system damage manifest as decreased CD4 T cell responses, a constricted repertoire of T cell antigen recognition, or as structural compromise of lymphoid tissue architecture can be reversed upon cessation of active HIV-1 replication by combinations of potent antiviral drugs.