CC CKRS: A RANTES, MIP-1 alpha, MIP-1 beta receptor as a fusion cofactor for macrophage-tropic HIV-1

被引:2392
作者
Alkhatib, G
Combadiere, C
Broder, CC
Feng, Y
Kennedy, PE
Murphy, PM
Berger, EA
机构
[1] NIAID,HOST DEF LAB,NIH,BETHESDA,MD 20892
[2] NIAID,VIRAL DIS LAB,NIH,BETHESDA,MD 20892
关键词
D O I
10.1126/science.272.5270.1955
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
Human immunodeficiency virus-type 1 (HIV-1) entry requires fusion cofactors on the CD4(+) target cell. Fusin, a heterotrimeric GTP-binding protein (G protein)-coupled receptor, serves as a cofactor for T cell line-tropic isolates. The chemokines RANTES, MIP-1 alpha, and MIP-1 beta, which suppress infection by macrophage-tropic isolates, selectively inhibited cell fusion mediated by the corresponding envelope glycoproteins (Envs). Recombinant CC CKR5, a G protein-coupled receptor for these chemokines, rendered CD4-expressing nonhuman cells fusion-competent preferentially with macrophage-tropic Envs. CC CKR5 messenger RNA was detected selectively in cell types susceptible to macrophage-tropic isolates. CC CKR5 is thus a fusion cofactor for macrophage-tropic HIV-1 strains.
引用
收藏
页码:1955 / 1958
页数:4
相关论文
共 32 条
[1]   REGULATED EXPRESSION OF FOREIGN GENES IN VACCINIA VIRUS UNDER THE CONTROL OF BACTERIOPHAGE-T7 RNA-POLYMERASE AND THE ESCHERICHIA-COLI LAC REPRESSOR [J].
ALEXANDER, WA ;
MOSS, B ;
FUERST, TR .
JOURNAL OF VIROLOGY, 1992, 66 (05) :2934-2942
[2]   Cell type-specific fusion cofactors determine human immunodeficiency virus type 1 tropism for T-cell lines versus primary macrophages [J].
Alkhatib, G ;
Broder, CC ;
Berger, EA .
JOURNAL OF VIROLOGY, 1996, 70 (08) :5487-5494
[3]   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
[4]  
BERGER EA, 1995, HIV PRACTICAL APPROA, V2, P123
[5]   THE BLOCK TO HIV-1 ENVELOPE GLYCOPROTEIN-MEDIATED MEMBRANE-FUSION IN ANIMAL-CELLS EXPRESSING HUMAN CD4 CAN BE OVERCOME BY A HUMAN CELL COMPONENT(S) [J].
BRODER, CC ;
DIMITROV, DS ;
BLUMENTHAL, R ;
BERGER, EA .
VIROLOGY, 1993, 193 (01) :483-491
[6]   FUSOGENIC SELECTIVITY OF THE ENVELOPE GLYCOPROTEIN IS A MAJOR DETERMINANT OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TROPISM FOR CD4(+) T-CELL LINES VS PRIMARY MACROPHAGES [J].
BRODER, CC ;
BERGER, EA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (19) :9004-9008
[7]   CD26 ANTIGEN AND HIV FUSION [J].
CALLEBAUT, C ;
JACOTOT, E ;
KRUST, B ;
HOVANESSIAN, AG .
SCIENCE, 1994, 264 (5162) :1162-1165
[8]  
CHAKRABARTI SK, COMMUNICATION
[9]   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
[10]   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