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Cytokine. 2001 Jan 7;13(1):55-59.

Tumor necrosis factor-alpha drives HIV-1 replication in U937 cell clones and upregulates CXCR4.

Author information

1
Laboaratory of Clinical Immunology, Scientific Institute H San Raffaele, Milan, Italy. Priscilla.Biswas@hsr.it

Abstract

U937 cell clones in which efficient (plus) vs poor (minus) replication of HIV-1 occurs have been described. We evaluated the role of host factors in their differential ability to support HIV-1 replication. Plus clones constitutively produced TNF-alpha and viral replication was inhibited by neutralization of endogenous TNF-alpha. However, HIV-1 replication was strongly upregulated in minus clones by exogenous TNF-alpha, which also further accelerated the kinetics of infection in plus clones. We observed an increased accumulation of proviral DNA within one round of HIV-1 replication following TNF-a treatment of plus cells. This effect was associated with increased surface density of CXCR4 in both plus and minus clones. Our results identify TNF-alpha as one correlate that contributes to the higher ability of U937-plus clones to sustain HIV-1 replication. Furthermore, we suggest that TNF-alpha may affect steps of the viral life cycle that occur earlier than transcription and also enhance HIV-1 replication by increasing the surface density of CXCR4.

PMID:
11145843
DOI:
10.1006/cyto.2000.0798
[Indexed for MEDLINE]

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