HIV-1 infection of macrophages promotes long-term survival and sustained release of interleukins 1 alpha and 6.

Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.

HIV-1 infection of macrophages promotes long-term survival and sustained release of interleukins 1 alpha and 6.

AIDS Res Hum Retroviruses. 1994 May;10(5):529-39. Unique Identifier : AIDSLINE MED/95000925
Berman MA; Zaldivar F Jr; Imfeld KL; Kenney JS; Sandborg CI; Department of Medicine, California College of Medicine,; University of California, Irvine 92717.

Abstract: HIV infection of macrophages in vivo may result in activation of monokine genes and cause persistent release of immunomodulatory and inflammatory cytokines. Studies that have examined cytokine (IL-1, IL-6, and TNF-alpha) activation by in vitro infection of normal peripheral blood mononuclear cells (PBMCs) with HIV-1 have produced conflicting results. The present study shows that for monokine induction by HIV-1-IIIB preparations derived from the H9 tumor cell line, partial purification of virus particles is essential. Infectious HIV-1 induces the release of high levels of IL-1 alpha, IL-1 beta, and IL-6 bioactivity by adherent PBMCs in the first 3 days following in vitro infection, but only IL-1 alpha and IL-6 continue to be released over several weeks of culture. High levels of bioactive IL-1 beta were released only up to 72 hr following infection, although intracellular IL-1 beta was detectable for at least 3 weeks. No TNF-alpha bioactivity or immunoreactive protein was detectable at > 48 hr in HIV-infected cultures. This time course of monokine release was dependent on the number of infectious particles added to PBMC cultures. In long-term cultures (> 1 month) HIV infection was found to promote the viability of macrophages. The finding of sustained release of IL-1 alpha and IL-6 by infected macrophages, without additional stimulation, suggests that these mediators are released by HIV-1-infected macrophages in AIDS patients, where they may interfere with proper immune regulation.

Keywords: Cell Survival Human HIV Infections/*IMMUNOLOGY/MICROBIOLOGY/PATHOLOGY HIV-1/*IMMUNOLOGY In Vitro Interleukin-1/*BIOSYNTHESIS Interleukin-6/*BIOSYNTHESIS Kinetics Macrophages/IMMUNOLOGY/MICROBIOLOGY/PATHOLOGY Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. T-Lymphocytes/MICROBIOLOGY Tumor Necrosis Factor/BIOSYNTHESIS JOURNAL ARTICLE
950130
M9510844

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