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CUTTING EDGE |
,§
Units of
*
Molecular Immunoregulation,
Human Virology, and
Immunobiology of HIV, DIBIT, San Raffaele Scientific Institute, Milan, Italy; and
§
Department of Biology and Genetics, University of Milan, Milan, Italy
The identification of HIV-1 coreceptors has provided a molecular
basis for the tropism of different HIV-1 strains. CXC chemokine
receptor-4 (CXCR4) mediates the entry of both primary and T cell
line-adapted (TCLA) syncytia-inducing strains. Although macrophages
(M
) express CXCR4, this coreceptor is assumed to be nonfunctional
for HIV-1 infection. We addressed this apparent paradox by infecting
human monocyte-derived M with primary and TCLA isolates that were
rigorously characterized for coreceptor usage and by adding the natural
CXCR4 ligand, stem cell differentiation factor-1, to specifically block
CXCR4-mediated entry. Our results show that primary HIV-1 isolates that
selectively use CXCR4 productively infected both normal and C-C
chemokine receptor-5-null M. By contrast, M supported the entry
of CXCR4-dependent TCLA strains with variable efficiency but were not
productively infected. Thus, the tropism of HIV isolates results from
complex virus/host cell interactions both at the entry and postentry
levels.
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