Exploitation of major histocompatibility complex class I molecules and caveolae by simian virus 40

被引:61
作者
Parton, RG [1 ]
Lindsay, M
机构
[1] Univ Queensland, Ctr Microscopy & Microanal, Dept Physiol & Pharmacol, Brisbane, Qld 4072, Australia
[2] Univ Queensland, Ctr Cellular & Mol Biol, Brisbane, Qld 4072, Australia
关键词
D O I
10.1111/j.1600-065X.1999.tb01280.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Simian virus 40 (SV40), a non-enveloped DNA virus, is transported from the cell surface to the nucleus where virus replication occurs. This pathway of virus uptake involves binding to surface MHC class I molecules, entry via non-coated pits, and subsequent transport to the endoplasmic reticulum (ER). At some stage in this pathway the virus must cross a membrane to reach the cytosol. In the present review the cellular machinery which the virus has utilized to enter the cell will be examined. In particular, we will consider recent evidence for the involvement of caveolae in the infectious entry step and propose a model involving recruitment of caveolar proteins around the membrane-bound virus. We also speculate that a similar mechanism may have been exploited by bacterial pathogens. The subsequent steps by which SV40 reaches the ER remain unclear but recent evidence suggests that this pathway may be shared with several other proteins that are transported from surface caveolae to the ER.
引用
收藏
页码:23 / 31
页数:9
相关论文
共 70 条
[1]   Bound simian virus 40 translocates to caveolin-enriched membrane domains, and its entry is inhibited by drugs that selectively disrupt caveolae [J].
Anderson, HA ;
Chen, YZ ;
Norkin, LC .
MOLECULAR BIOLOGY OF THE CELL, 1996, 7 (11) :1825-1834
[2]   MHC class I molecules are enriched in caveolae but do not enter with simian virus 40 [J].
Anderson, HA ;
Chen, YZ ;
Norkin, LC .
JOURNAL OF GENERAL VIROLOGY, 1998, 79 :1469-1477
[3]  
Anderson R G, 1993, Trends Cell Biol, V3, P177, DOI 10.1016/0962-8924(93)90205-F
[4]   The caveolae membrane system [J].
Anderson, RGW .
ANNUAL REVIEW OF BIOCHEMISTRY, 1998, 67 :199-225
[5]   CLASS-I MAJOR HISTOCOMPATIBILITY PROTEINS AS CELL-SURFACE RECEPTORS FOR SIMIAN VIRUS-40 [J].
ATWOOD, WJ ;
NORKIN, LC .
JOURNAL OF VIROLOGY, 1989, 63 (10) :4474-4477
[6]   Survival of FimH-expressing enterobacteria in macrophages relies on glycolipid traffic [J].
Baorto, DM ;
Gao, ZM ;
Malaviya, R ;
Dustin, ML ;
vanderMerwe, A ;
Lublin, DM ;
Abraham, SN .
NATURE, 1997, 389 (6651) :636-639
[7]   EXPRESSION OF SV40 RECEPTORS ON APICAL SURFACES OF POLARIZED EPITHELIAL-CELLS [J].
BASAK, S ;
TURNER, H ;
COMPANS, RW .
VIROLOGY, 1992, 190 (01) :393-402
[8]   AUTOCRINE MOTILITY FACTOR-RECEPTOR IS A MARKER FOR A DISTINCT MEMBRANOUS TUBULAR ORGANELLE [J].
BENLIMAME, N ;
SIMARD, D ;
NABI, IR .
JOURNAL OF CELL BIOLOGY, 1995, 129 (02) :459-471
[9]   Localization of autocrine motility factor receptor to caveolae and clathrin-independent internalization of its ligand to smooth endoplasmic reticulum [J].
Benlimame, N ;
Le, PU ;
Nabi, IR .
MOLECULAR BIOLOGY OF THE CELL, 1998, 9 (07) :1773-1786
[10]   CLASS-I MAJOR HISTOCOMPATIBILITY PROTEINS ARE AN ESSENTIAL COMPONENT OF THE SIMIAN VIRUS-40 RECEPTOR [J].
BREAU, WC ;
ATWOOD, WJ ;
NORKIN, LC .
JOURNAL OF VIROLOGY, 1992, 66 (04) :2037-2045