IS CD4 SUFFICIENT FOR HIV ENTRY - CELL-SURFACE MOLECULES INVOLVED IN HIV-INFECTION

被引：11

作者：

CLAPHAM, P

MCKNIGHT, A

SIMMONS, G

WEISS, R

机构：

[1] Chester Beatty Laboratories, Institute of Cancer Research, London

来源：

PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES | 1993年 / 342卷 / 1299期

基金：

英国医学研究理事会;

关键词：

D O I：

10.1098/rstb.1993.0137

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

HIV-1, HIV-2 and SIV each bind to CD4 as the first step in virus entry. However, alternative receptors may also be used. HIV-1 binds to glycolipids with terminal galactosylceramide residues on neural cells; opsonized virus binds to Fc receptors; HIV-2 can infect certain CD4-negative cells. Further receptors may also play a role in CD4-mediated infection, including cell adhesion molecules and possibly cell surface proteinases. After binding to CD4, immunodeficiency viruses require secondary molecules to effect fusion between the virus envelope and the cell membrane; these accessory requirements differ between HIV-1, HIV-2 and SIV.

引用

收藏

页码：67 / 73

页数：7

相关论文

共 50 条

[11] THE V3 LOOPS OF THE HIV-1 AND HIV-2 SURFACE GLYCOPROTEINS CONTAIN PROTEOLYTIC CLEAVAGE SITES - A POSSIBLE FUNCTION IN VIRAL FUSION [J].

CLEMENTS, GJ ;

PRICEJONES, MJ ;

STEPHENS, PE ;

SUTTON, C ;

SCHULZ, TF ;

CLAPHAM, PR ;

MCKEATING, JA ;

MCCLURE, MO ;

THOMSON, S ;

MARSH, M ;

KAY, J ;

WEISS, RA ;

MOORE, JP .

AIDS RESEARCH AND HUMAN RETROVIRUSES, 1991, 7 (01) :3-16

[12] SINGLE AMINO-ACID CHANGES IN HIV ENVELOPE AFFECT VIRAL TROPISM AND RECEPTOR-BINDING [J].

CORDONNIER, A ;

MONTAGNIER, L ;

EMERMAN, M .

NATURE, 1989, 340 (6234) :571-574

[13] SEQUENCE AND EXPRESSION OF A MEMBRANE-ASSOCIATED C-TYPE LECTIN THAT EXHIBITS CD4-INDEPENDENT BINDING OF HUMAN-IMMUNODEFICIENCY-VIRUS ENVELOPE GLYCOPROTEIN-GP120 [J].

CURTIS, BM ;

SCHARNOWSKE, S ;

WATSON, AJ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (17) :8356-8360

[14] THE CD4 (T4) ANTIGEN IS AN ESSENTIAL COMPONENT OF THE RECEPTOR FOR THE AIDS RETROVIRUS [J].

DALGLEISH, AG ;

BEVERLEY, PCL ;

CLAPHAM, PR ;

CRAWFORD, DH ;

GREAVES, MF ;

WEISS, RA .

NATURE, 1984, 312 (5996) :763-767

[15]

DRAJIC T, 1992, J VIROL, V66, P4794

[16]

DVEKSLER GS, 1993, J VIROL, V67, P1

[17] HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ACTIVATES THE CLASSICAL PATHWAY OF COMPLEMENT BY DIRECT C1-BINDING THROUGH SPECIFIC SITES IN THE TRANSMEMBRANE GLYCOPROTEIN-GP41 [J].

EBENBICHLER, CF ;

THIELENS, NM ;

VORNHAGEN, R ;

MARSCHANG, P ;

ARLAUD, GJ ;

DIERICH, MP .

JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 174 (06) :1417-1424

[18]

FENYO EM, 1988, J VIROL, V62, P4414

[19] THE MAJOR HUMAN RHINOVIRUS RECEPTOR IS ICAM-1 [J].

GREVE, JM ;

DAVIS, G ;

MEYER, AM ;

FORTE, CP ;

YOST, SC ;

MARIOR, CW ;

KAMARCK, ME ;

MCCLELLAND, A .

CELL, 1989, 56 (05) :839-847

[20] REEVALUATION OF THE INVOLVEMENT OF THE ADHESION MOLECULES ICAM-1/LFA-1 IN SYNCYTIA FORMATION OF HIV-1-INFECTED SUBCLONES OF A CEM T-CELL LEUKEMIC LINE [J].

GRUBER, MF ;

WEBB, DSA ;

GERRARD, TL ;

MOSTOWSKI, HS ;

VUJCIC, L ;

GOLDING, H .

AIDS RESEARCH AND HUMAN RETROVIRUSES, 1991, 7 (01) :45-53

← 1 2 3 4 5 →