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. In 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.
Wahl
S M
SM
Oral Infection and Immunity Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892-4352, USA.
Orenstein
J M
JM
D017088:AIDS-Related Opportunistic Infections / Q000276:immunology*; D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000821:virology; D018450:Disease Progression; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D008264:Macrophages / Q000276:immunology* / Q000821:virology; D014766:Viremia / Q000276:immunology; D014779:Virus Replication