Escape of non-enveloped virus from intact cells

被引:55
作者
Bird, Sara W. [1 ]
Kirkegaard, Karla [1 ,2 ]
机构
[1] Stanford Univ, Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA
[2] Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA
基金
美国国家卫生研究院;
关键词
Unconventional secretion; Multi-vesicular bodies; Autophagy; Viral spread; Picornavirus; UNCONVENTIONAL SECRETION; PERSISTENT INFECTION; AUTOPHAGY; RELEASE; POLIOVIRUS; PROTEIN; SPREAD; ACB1;
D O I
10.1016/j.virol.2015.03.044
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
How do viruses spread from cell to cell? Enveloped viruses acquire their surrounding membranes by budding. If a newly enveloped virus has budded through the plasma membrane, it finds itself outside the cell immediately. If it has budded through the bounding membrane of an internal compartment such as the ER, the virus finds itself in the lumen, from which it can exit the cell via the conventional secretion pathway. Thus, although some enveloped viruses destroy the cells they infect, there is no topological need to do so. On the other hand, naked viruses such as poliovirus lack an external membrane. They are protein-nucleic acid complexes within the cytoplasm or nucleus of the infected cell, like a ribosome, a spliceosome or an aggregate of Huntingtin protein. The simplest way for such a particle to pass through the single lipid bilayer that separates it from the outside of the cell would be to violate the integrity of that bilayer. Thus, it is not surprising that the primary mode of exit for non-enveloped viruses is cell lysis. However, more complex exit strategies are possible, such as the creation of new compartments whose complex topologies allow the exit of cytoplasm and its contents without violating the integrity of the cell. Here we will discuss the non-lytic spread of poliovirus and recent observations of such compartments during viral infection with several different picornaviruses. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:444 / 449
页数:6
相关论文
共 29 条
[1]   The Transcellular Spread of Cytosolic Amyloids, Prions, and Prionoids [J].
Aguzzi, Adriano ;
Rajendran, Lawrence .
NEURON, 2009, 64 (06) :783-790
[2]   Pancreatic Acinar Cell-Specific Autophagy Disruption Reduces Coxsackievirus Replication and Pathogenesis In Vivo [J].
Alirezaei, Mehrdad ;
Flynn, Claudia T. ;
Wood, Malcolm R. ;
Whitton, J. Lindsay .
CELL HOST & MICROBE, 2012, 11 (03) :298-305
[3]   Nonlytic viral spread enhanced by autophagy components [J].
Bird, Sara Whitney ;
Maynard, Nathaniel D. ;
Covert, Markus W. ;
Kirkegaard, Karla .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2014, 111 (36) :13081-13086
[4]  
Choi AMK, 2013, NEW ENGL J MED, V368, P1845, DOI [10.1056/NEJMra1205406, 10.1056/NEJMc1303158]
[5]   RELEASE OF SIMIAN VIRUS-40 VIRIONS FROM EPITHELIAL-CELLS IS POLARIZED AND OCCURS WITHOUT CELL-LYSIS [J].
CLAYSON, ET ;
BRANDO, LVJ ;
COMPANS, RW .
JOURNAL OF VIROLOGY, 1989, 63 (05) :2278-2288
[6]   PERSISTENT POLIOVIRUS INFECTION OF HUMAN NEURO-BLASTOMA CELLS [J].
COLBEREGARAPIN, F ;
CHRISTODOULOU, C ;
CRAINIC, R ;
PELLETIER, I .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (19) :7590-7594
[7]   ELECTRON MICROSCOPIC STUDY OF FORMATION OF POLIOVIRUS [J].
DALES, S ;
EGGERS, HJ ;
TAMM, I ;
PALADE, GE .
VIROLOGY, 1965, 26 (03) :379-&
[8]   Autophagy in infection, inflammation and immunity [J].
Deretic, Vojo ;
Saitoh, Tatsuya ;
Akira, Shizuo .
NATURE REVIEWS IMMUNOLOGY, 2013, 13 (10) :722-737
[9]   CORRELATION OF THE STAGE OF CYTOPATHIC CHANGE WITH THE RELEASE OF POLIOMYELITIS VIRUS [J].
DUNNEBACKE, TH .
VIROLOGY, 1956, 2 (03) :399-410
[10]   Unconventional secretion of Acb1 is mediated by autophagosomes [J].
Duran, Juan M. ;
Anjard, Christophe ;
Stefan, Chris ;
Loomis, William F. ;
Malhotra, Vivek .
JOURNAL OF CELL BIOLOGY, 2010, 188 (04) :527-536