Abstract
BackgroundCellular infection with human immunodeficiency virus (HIV) both in vitro and in vivo requires a member of the chemokine receptor family to act as a co-receptor for viral entry. However, it is presently unclear to what extent the interaction of HIV proteins with chemokine receptors generates intracellular signals that are important for productive infection.ResultsIn this study we have used a recently described family of chemokine inhibitors, termed BSCIs, which specifically block chemokine-induced chemotaxis without affecting chemokine ligands binding to their receptors. The BSCI termed Peptide 3 strongly inhibited CCR5 mediated HIV infection of THP-1 cells (83 ± 7% inhibition assayed by immunofluoresence staining), but had no effect on gp120 binding to CCR5. Peptide 3 did not affect CXCR4-dependent infection of Jurkat T cells.ConclusionThese observations suggest that, in some cases, intracellular signals generated by the chemokine coreceptor may be required for a productive HIV infection.
Highlights
Cellular infection with human immunodeficiency virus (HIV) both in vitro and in vivo requires a member of the chemokine receptor family to act as a co-receptor for viral entry
Specific binding of gp120:V3(BaL) to Jurkat cells was not detected even at concentrations up to 500 μM (Fig 1a). These observations are consistent with the hypothesis that gp120:V3(BaL) binds to CCR5, which is expressed on the surface of THP-1 monocytic cells but not on Jurkat T-cells
There was approximately 5-fold greater specific binding to the Jurkat cells than the THP-1 cells (Fig 1b). These observations are consistent with the hypothesis that gp120:V3(IIIb) binds to CXCR4, which is expressed on both THP-1 and Jurkat cells, but at higher levels on the T-cell line
Summary
Cellular infection with human immunodeficiency virus (HIV) both in vitro and in vivo requires a member of the chemokine receptor family to act as a co-receptor for viral entry. It is presently unclear to what extent the interaction of HIV proteins with chemokine receptors generates intracellular signals that are important for productive infection. The HIV gp120 protein which interacts with the chemokine co-receptor primarily through its V3 loop can induce leukocyte chemotaxis, demonstrating that some intracellular signals are generated through the the virus:receptor interaction [17,18]. This signalling occurs (page number not for citation purposes)
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