Document 0972 DOCN M9470972 TI Enhancement of HIV-1 replication in peripheral blood mononuclear cells by Cryptococcus neoformans is monocyte-dependent but tumour necrosis factor-independent. DT 9409 AU Orendi JM; Nottet HS; Visser MR; Verheul AF; Snippe H; Verhoef J; Department of Clinical Microbiology, University Hospital Utrecht,; The Netherlands. SO AIDS. 1994 Apr;8(4):423-9. Unique Identifier : AIDSLINE MED/94280713 AB 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. DE Antibodies, Monoclonal/IMMUNOLOGY Cells, Cultured Cryptococcus neoformans/*PHYSIOLOGY Human HIV-1/*PHYSIOLOGY Monocytes/CYTOLOGY/*MICROBIOLOGY/PHYSIOLOGY Pentoxifylline/PHARMACOLOGY Tumor Necrosis Factor/IMMUNOLOGY/*METABOLISM Virus Replication JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).