HIV-1 entry into CD4 sup + cells is mediated by the chemokine receptor CC-CKR-5.
Dragic, Tatjana; Litwin, Virginia; Allaway, Graham P.; Martin, Scott R.; Huang, Yaoxing; Nagashima, Kirsten A.; Cayanan, Charmagne; Maddon, Paul J.; Koup, Richard A.; Moore John P.; Paxton, William A.
[Article]
Nature.
381(6584):667-673, June 20, 1996.
(Format: HTML)
The beta-chemokines MIP-1 alpha, MIP-1 beta and RANTES inhibit infection of CD4 sup T cells by primary, non-syncytium-inducing (NSI) HIV-1 strains at the virus entry stage, and also block env-mediated cell-cell membrane fusion. CD4 sup T cells from some HIV-1-exposed uninfected individuals cannot fuse with NSI HIV-1 strains and secrete high levels of beta-chemokines. Expression of the beta-chemokine receptor CC-CKR-5 in CD4 sup non-permissive human and non-human renders them susceptible to infection by NSI strains, and allows env-mediated membrane fusion. CC-CKR-5 is a second receptor for NSI primary viruses.
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