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Immune stimulation and HIV‐1 viral replication
Author(s) -
Wahl Sharon M.,
Orenstein Jan M.
Publication year - 1997
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.62.1.67
Subject(s) - biology , immune system , viral replication , replication (statistics) , virology , stimulation , human immunodeficiency virus (hiv) , immunology , microbiology and biotechnology , virus , neuroscience
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. J. Leukoc. Biol . 62: 67–71, 1997.