Impairment of phagosome-lysosome fusion in HIV-1-infected macrophages

J Acquir Immune Defic Syndr Hum Retrovirol. 1996 Sep;13(1):18-22. doi: 10.1097/00042560-199609000-00003.

Abstract

Phagosome-lysosome fusion is critical for intracellular killing of most organisms and is inhibited by some viruses, notably influenza. We explored the effects of infection in vitro with HIV-1 (IIIB or Ada-M) on phagosome-lysosome fusion in blood monocyte-derived macrophages. After 8 days of infection, fusion was assessed from the fluorescence change occurring up to 2 h after labeling the lysosome compartment with acridine orange and loading of phagosomes with opsonized yeast. Compared with mock-infected control macrophages, the proportion of cells showing fusion after infection was reduced from a mean of 70% to a mean of 47% (p = 0.0001). Inhibition was seen with heat-killed HIV-1 IIIB but not virus-free filtrate. It was mimicked by recombinant gp 120 and blocked by soluble CD4 or antibody to CD4 but not by a neutralizing antibody to the V3 loop of gp 120. The inhibitory effect was seen 8 days after the original, transient exposure to gp 120. These results suggest that a lasting abnormality of phagosome-lysosome fusion results from interaction between gp 120 and CD4, contributing, perhaps, to the increased susceptibility to opportunistic infections of people infected with HIV.

Publication types

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

MeSH terms

  • CD4 Antigens / immunology
  • CD4 Antigens / metabolism
  • Cells, Cultured
  • HIV Envelope Protein gp120 / immunology
  • HIV Envelope Protein gp120 / physiology
  • HIV Infections / virology*
  • HIV-1*
  • Humans
  • Macrophages / physiology*
  • Macrophages / virology*
  • Microscopy, Fluorescence
  • Phagocytosis / physiology*
  • Phagosomes / physiology*
  • Phagosomes / virology

Substances

  • CD4 Antigens
  • HIV Envelope Protein gp120