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1
*
Department of Molecular Microbiology and Immunology, Johns Hopkins School of Hygiene and Public Health, Baltimore, MD 21205;
Department of Pharmacology and Molecular Science, Johns Hopkins School of Medicine, Baltimore, MD 21205; and
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110
HIV-1 infection of human PBMC has been shown to elicit secretion of
several different cytokines. TNF-
secretion induced by this virus
has been of particular interest because it has been associated with the
development of HIV-1 dementia and because TNF- increases viral
replication by enhancing NF-
B interaction with the viral promoter,
the HIV-1 long terminal repeat. Thus, an autocrine pathway is
potentially created in which HIV-1 stimulates its own replication.
Conflicting reports exist, however, on the ability of HIV-1 to induce
TNF- secretion in vitro or in vivo. Using experimental protocols
that controlled for potential bacterial endotoxin-induced TNF-
secretion, the current study demonstrates significant differences in
TNF--eliciting properties among primary and laboratory obtained
HIV-1. The relative TNF--inducing ability of different variants is
conserved when tested using PBMC from different individuals.
Elicitation of TNF- secretion was not blocked by exposure of cells
to zidovudine, indicating that viral integration was not required to
induce secretion. Rather, the interaction between the virus and cell
surface is critical for TNF- induction, as Abs against CD4 or CCR5
blocked the induction of TNF- synthesis by PBMC when added before
virus exposure. Furthermore, the ability to induce TNF- secretion
mapped to a region of the HIV-1 env gene that includes
the third hypervariable domain. Differences in the ability of different
HIV-1 variants to elicit TNF- may account for individual differences
in HIV-1 disease course.
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