Characterization of a macrophage-tropic HIV strain that does not alter macrophage cytokine production yet protects macrophages from superinfection by vesicular stomatitis virus

AIDS Res Hum Retroviruses. 1990 Aug;6(8):1023-6. doi: 10.1089/aid.1990.6.1023.

Abstract

Macrophages, unlike CD4+ T cells, can be productively infected by human immunodeficiency virus (HIV) without prior cellular activation. Cytopathic infection ensues without the induction of tumor necrosis factor alpha (TNF alpha), interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), or tissue factor genes. In detailed studies on TNF alpha, HIV infection did not affect the regulation of TNF alpha in response to bacterial lipopolysaccharide. In an effort to examine the interferon responsiveness of HIV-infected macrophages, the cells were challenged with vesicular stomatitis virus (VSV) with or without interferon pretreatment. Surprisingly, HIV-infected macrophages were completely resistant to VSV-induced lysis even in the absence of interferon; however, no interferon was detected in the supernatants of these infected cells. The resistance of HIV-infected macrophages to superinfection with VSV indicates a previously undescribed effect of HIV upon macrophage cellular metabolism.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acquired Immunodeficiency Syndrome / complications
  • Acquired Immunodeficiency Syndrome / immunology*
  • Cells, Cultured
  • Cytokines / biosynthesis*
  • Gene Expression Regulation, Viral
  • HIV-1 / pathogenicity*
  • Humans
  • Interleukins / biosynthesis
  • Interleukins / genetics
  • Macrophage Activation
  • Macrophages / immunology*
  • Macrophages / microbiology
  • Monocytes / immunology
  • Stomatitis / complications
  • Stomatitis / immunology*
  • Superinfection / immunology*
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / genetics
  • Vesicular stomatitis Indiana virus / pathogenicity*
  • Virus Diseases / complications
  • Virus Diseases / immunology*

Substances

  • Cytokines
  • Interleukins
  • Tumor Necrosis Factor-alpha