Identification of a major co-receptor for primary isolates of HIV-1

被引:3138
作者
Deng, HK
Liu, R
Ellmeier, W
Choe, S
Unutmaz, D
Burkhart, M
DiMarzio, P
Marmon, S
Sutton, RE
Hill, CM
Davis, CB
Peiper, SC
Schall, TJ
Littman, DR
Landau, NR
机构
[1] NYU,MED CTR,SKIRBALL INST BIOMOL MED,NEW YORK,NY 10016
[2] NYU,MED CTR,HOWARD HUGHES MED INST,NEW YORK,NY 10016
[3] ROCKEFELLER UNIV,AARON DIAMOND AIDS RES CTR,NEW YORK,NY 10016
[4] STANFORD UNIV,MED CTR,DEPT BIOCHEM,STANFORD,CA 94305
[5] UNIV LOUISVILLE,SCH MED,JAMES GRAHAM BROWN CANC CTR,LOUISVILLE,KY 40207
[6] DNAX RES INST MOLEC & CELLULAR BIOL INC,DEPT IMMUNOL,PALO ALTO,CA 94304
关键词
D O I
10.1038/381661a0
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
Entry of HIV-1 into target cells requires cell-surface CD4 and additional host cell cofactors. A cofactor required for infection with virus adapted for growth in transformed T-cell lines was recently identified and named fusin. However, fusin does not promote entry of macrophage-tropic viruses, which are believed to be the key pathogenic strains in vivo. The principal cofactor for entry mediated by the envelope glycoproteins of primary macrophage-tropic strains of HIV-1 is CC-CKR-5, a receptor for the beta-chemokines RANTES, MIP-1 alpha and MIP-1 beta.
引用
收藏
页码:661 / 666
页数:6
相关论文
共 44 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]   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
[3]   STRUCTURE OF INFLUENZA HEMAGGLUTININ AT THE PH OF MEMBRANE-FUSION [J].
BULLOUGH, PA ;
HUGHSON, FM ;
SKEHEL, JJ ;
WILEY, DC .
NATURE, 1994, 371 (6492) :37-43
[4]  
CHAUDHURI A, 1994, J BIOL CHEM, V269, P7835
[5]   ISOLATES OF HUMAN IMMUNODEFICIENCY VIRUS TYPE-1 FROM THE BRAIN MAY CONSTITUTE A SPECIAL GROUP OF THE AIDS VIRUS [J].
CHENGMAYER, C ;
WEISS, C ;
SETO, D ;
LEVY, JA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (21) :8575-8579
[6]   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
[7]   IDENTIFICATION OF RANTES, MIP-1-ALPHA, AND MIP-1-BETA AS THE MAJOR HIV-SUPPRESSIVE FACTORS PRODUCED BY CD8(+) T-CELLS [J].
COCCHI, F ;
DEVICO, AL ;
GARZINODEMO, A ;
ARYA, SK ;
GALLO, RC ;
LUSSO, P .
SCIENCE, 1995, 270 (5243) :1811-1815
[8]   CLONING AND FUNCTIONAL EXPRESSION OF A HUMAN EOSINOPHIL CC-CHEMOKINE RECEPTOR [J].
COMBADIERE, C ;
AHUJA, SK ;
MURPHY, PM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (28) :16491-16494
[9]  
COMELISSEN M, 1995, J VIROL, V69, P1810
[10]   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