HIV-1 entry into CD4(+) cells is mediated by the chemokine receptor CC-CKR-5

被引:2777
作者
Dragic, T
Litwin, V
Allaway, GP
Martin, SR
Huang, YX
Nagashima, KA
Cayanan, C
Maddon, PJ
Koup, RA
Moore, JP
Paxton, WA
机构
[1] ROCKEFELLER UNIV,AARON DIAMOND AIDS RES CTR,NEW YORK,NY 10016
[2] PROGEN PHARMACEUT INC,TARRYTOWN,NY 10591
关键词
D O I
10.1038/381667a0
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The beta-chemokines MIP-1 alpha, MIP-1 beta and RANTES inhibit infection of CD4(+) 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(+) 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(+), non-permissive human and non-human cells 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.
引用
收藏
页码:667 / 673
页数:7
相关论文
共 29 条