Immune stimulation and HIV-1 viral replication

A biphasic early and late viremia is characteristic of HIV-1 infection, The first increase in circulating viral burden occurs within weeks after infection, before a host immune response, and the second, later peak emerges during the inevitable HIV-1 devastation of immune function, Recently, intermittent bouts of viremia have also been identified in HIV-1-infected individuals and found to be associated with episodes of immune challenge, Vaccinations, exposure to antigens, and infections often induce reversible increases in circulating viral levels, dependent on CD4(+) T lymphocyte numbers, However, even with marked losses in CD4(+) T cell counts, opportunistic infections appear to trigger a viremic response, ln searching for the source of this virus, macrophages in tissues co-infected with opportunistic pathogens have been identified as prodigious producers of HIV-1, Thus, the fountain from which HIV-1 emerges may shift from CD4(+) T lymphocytes in early HIV-1 infection to tissue macrophages later in the natural evolution of the disease, as the CD4(+) T cells are depleted, Defining the mechanisms of this transitional event in HIV-1 infection may facilitate regulation and therapeutic control of both opportunistic infections and HIV-1.