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A dual-tropic primary HIV-1 isolate that uses fusin and the beta-chemokine receptors CKR-5, CKR-3, and CKR-2b as fusion cofactors.

Abstract：

:Here, we show that the beta-chemokine receptor CKR-5 serves as a cofactor for M-tropic HIV viruses. Expression of CKR-5 with CD4 enables nonpermissive cells to form syncytia with cells expressing M-tropic, but not T-tropic, HIV-1 env proteins. Expression of CKR-5 and CD4 enables entry of a M-tropic, but not a T-tropic, virus strain. A dual-tropic primary HIV-1 isolate (89.6) utilizes both Fusin and CKR-5 as entry cofactors. Cells expressing the 89.6 env protein form syncytia with QT6 cells expressing CD4 and either Fusin or CKR-5. The beta-chemokine receptors CKR-3 and CKR-2b support HIV-1 89.6 env-mediated syncytia formation but do not support fusion by any of the T-tropic or M-tropic strains tested. Our results suggest that the T-tropic viruses characteristic of disease progression may evolve from purely M-tropic viruses prevalent early in virus infection through changes in the env protein that enable the virus to use multiple entry cofactors.

journal_name

Cell

journal_title

Cell

authors

Doranz BJ,Rucker J,Yi Y,Smyth RJ,Samson M,Peiper SC,Parmentier M,Collman RG,Doms RW

doi

10.1016/s0092-8674(00)81314-8

subject

Has Abstract

pub_date

1996-06-28 00:00:00

pages

1149-58

issue

7

eissn

0092-8674

issn

1097-4172

pii

S0092-8674(00)81314-8

journal_volume

85

pub_type

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