Enhancement of HIV-1 replication in peripheral blood mononuclear cells by Cryptococcus neoformans is monocyte-dependent but tumour necrosis factor-independent

AIDS. 1994 Apr;8(4):423-9. doi: 10.1097/00002030-199404000-00003.

Abstract

Objective: To investigate the possible role of Cryptococcus neoformans in HIV-1 pathogenesis.

Design: An in vitro system was developed to study HIV-1 replication in freshly HIV-1-infected peripheral blood mononuclear cells (PBMC) incubated with whole azide-killed C. neoformans.

Methods: Human PBMC or peripheral blood lymphocytes were infected with lymphocytotropic HIV-1 and incubated with azide-killed encapsulated or non-encapsulated C. neoformans for 10 days. Viral replication was followed by HIV-1 p24 enzyme-linked immunosorbent assay and median tissue culture infective dose determination. Tumour necrosis factor (TNF) release by PBMC, induced by C. neoformans, was measured. Anti-TNF monoclonal antibodies or pentoxifylline were used to inhibit TNF bioactivity.

Results: Both encapsulated and non-encapsulated C. neoformans enhanced HIV-1 replication in PBMC but not in peripheral blood lymphocytes. C. neoformans induced TNF release by PBMC. Inhibition of TNF bioactivity did not block C. neoformans-enhanced HIV-1 replication in PBMC.

Conclusions: C. neoformans can enhance HIV-1 replication in T cells only in the presence of monocytic cells. This enhancement is not dependent on encapsulation nor can it be attributed to TNF release.

MeSH terms

  • Antibodies, Monoclonal / immunology
  • Cells, Cultured
  • Cryptococcus neoformans / physiology*
  • HIV-1 / physiology*
  • Humans
  • Monocytes / cytology
  • Monocytes / microbiology*
  • Monocytes / physiology
  • Pentoxifylline / pharmacology
  • Tumor Necrosis Factor-alpha / immunology
  • Tumor Necrosis Factor-alpha / metabolism*
  • Virus Replication

Substances

  • Antibodies, Monoclonal
  • Tumor Necrosis Factor-alpha
  • Pentoxifylline