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-α and viral replication was inhibited by neutralization of endogenous TNF-α. However, HIV-1 replication was strongly upregulated in minus clones by exogenous TNF-α, 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-α as one correlate that contributes to the higher ability of U937-plus clones to sustain HIV-1 replication. Furthermore, we suggest that TNF-α 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.
Original language | English |
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Pages (from-to) | 55-59 |
Number of pages | 5 |
Journal | Cytokine |
Volume | 13 |
Issue number | 1 |
DOIs | |
Publication status | Published - Jan 7 2001 |
Keywords
- CXCR4
- HIV-1
- TNF-α
- U937
ASJC Scopus subject areas
- Endocrinology
- Molecular Biology
- Immunology
- Immunology and Allergy