In sexual transmission of simian immunodeficiency virus, and early and late
r stages of human immunodeficiency virus-type 1 (HIV-1) infection, both vir
uses were found to replicate predominantly in CD4(+) T cells at the portal
of entry and in Lymphoid tissues, infection was propagated not only in acti
vated and proliferating T cells but also, surprisingly, in resting T cells.
The infected proliferating cells correspond to the short-lived population
that produces the bulk of HIV-1. Most of the HIV-1-infected resting T cells
persisted after antiretroviral therapy. Latently and chronically infected
cells that may be derived from this population pose challenges to eradicati
ng infection and developing an effective vaccine.