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

被引:2781
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
[1]   HUMAN-IMMUNODEFICIENCY-VIRUS ENVELOPE GLYCOPROTEIN CD4-MEDIATED FUSION OF NONPRIMATE CELLS WITH HUMAN-CELLS [J].
ASHORN, PA ;
BERGER, EA ;
MOSS, B .
JOURNAL OF VIROLOGY, 1990, 64 (05) :2149-2156
[2]   ACTIVATION OF DUAL T-CELL SIGNALING PATHWAYS BY THE CHEMOKINE RANTES [J].
BACON, KB ;
PREMACK, BA ;
GARDNER, P ;
SCHALL, TJ .
SCIENCE, 1995, 269 (5231) :1727-1730
[3]   MONOCYTE CHEMOTACTIC PROTEIN-3 (MCP3) INTERACTS WITH MULTIPLE LEUKOCYTE RECEPTORS - C-C-CKR1, A RECEPTOR FOR MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA, RANTES, IS ALSO A FUNCTIONAL RECEPTOR FOR MCP3 [J].
BENBARUCH, A ;
XU, LL ;
YOUNG, PR ;
BENGALI, K ;
OPPENHEIM, JJ ;
WANG, JM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (38) :22123-22128
[4]   MOLECULAR-CLONING AND FUNCTIONAL EXPRESSION OF 2 MONOCYTE CHEMOATTRACTANT PROTEIN-1 RECEPTORS REVEALS ALTERNATIVE SPLICING OF THE CARBOXYL-TERMINAL TAILS [J].
CHARO, IF ;
MYERS, SJ ;
HERMAN, A ;
FRANCI, C ;
CONNOLLY, AJ ;
COUGHLIN, SR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (07) :2752-2756
[5]  
CHAUDHURI A, 1994, J BIOL CHEM, V269, P7835
[6]   DISTINCT MODES OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 PROVIRAL LATENCY REVEALED BY SUPERINFECTION OF NONPRODUCTIVELY INFECTED CELL-LINES WITH RECOMBINANT LUCIFERASE-ENCODING VIRUSES [J].
CHEN, BK ;
SAKSELA, K ;
ANDINO, R ;
BALTIMORE, D .
JOURNAL OF VIROLOGY, 1994, 68 (02) :654-660
[7]   SPECIFIC CELL-SURFACE REQUIREMENTS FOR THE INFECTION OF CD4-POSITIVE CELLS BY HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 AND TYPE-2 AND BY SIMIAN IMMUNODEFICIENCY VIRUS [J].
CLAPHAM, PR ;
BLANC, D ;
WEISS, RA .
VIROLOGY, 1991, 181 (02) :703-715
[8]  
COMBADIERE C, 1995, J BIOL CHEM, V270, P29671
[9]   HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 VARIANTS WITH INCREASED REPLICATIVE CAPACITY DEVELOP DURING THE ASYMPTOMATIC STAGE BEFORE DISEASE PROGRESSION [J].
CONNOR, RI ;
HO, DD .
JOURNAL OF VIROLOGY, 1994, 68 (07) :4400-4408
[10]   VPR IS REQUIRED FOR EFFICIENT REPLICATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 IN MONONUCLEAR PHAGOCYTES [J].
CONNOR, RI ;
CHEN, BK ;
CHOE, S ;
LANDAU, NR .
VIROLOGY, 1995, 206 (02) :935-944