Viruses and autophagy

被引:233
作者
Kudchodkar, Sagar B. [2 ]
Levine, Beth [1 ,2 ,3 ]
机构
[1] Univ Texas SW Med Ctr Dallas, Howard Hughes Med Inst, Dallas, TX 75390 USA
[2] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA
[3] Univ Texas SW Med Ctr Dallas, Dept Microbiol, Dallas, TX 75390 USA
关键词
HERPES-SIMPLEX-VIRUS; HEPATITIS-C VIRUS; BECLIN; CELL-DEATH; CORONAVIRUS REPLICATION; REGULATES AUTOPHAGY; PROTEIN; DEGRADATION; INFECTION; PHOSPHORYLATION;
D O I
10.1002/rmv.630
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Autophagy is an evolutionarily conserved intracellular process by which bulk cytoplasm is enveloped inside a double-membraned vesicle and shuttled to lysosomes for degradation. Within the last 15 years, the genes necessary for the execution of autophagy have been identified and the number of tools for studying this process has grown. Autophagy is essential for tissue homeostasis and development and defective autophagy is associated with a number of diseases. As intracellular parasites, during the course of an infection, viruses encounter autophagy and interact with the proteins that execute this process. Autophagy and/or autophagy genes likely play both anti-viral and proviral roles in the life cycles and pathogenesis of many different virus families. With respect to anti-viral roles, the autophagy proteins function in targeting viral components or virions for lysosomal degradation in a process termed xenophagy, and they also play a role in the initiation of innate and adaptive immune system responses to viral infections. Consistent with this anti-viral role of host autophagy, some viruses encode virulence factors that interact with the host autophagy machinery and block the execution of autophagy. In contrast, other viruses appear to Utilise components of the autophagic machinery to foster their own intracellular growth or non-lytic cellular egress. As the details of the role(s) of autophagy in viral pathogenesis become clearer, new anti-viral therapies could be developed to inhibit the beneficial and enhance the destructive aspects of autophagy on the viral life cycle. Copyright (C) 2009 John Wiley & Sons, Ltd.
引用
收藏
页码:359 / 378
页数:20
相关论文
共 117 条
[21]   Autophagy enhances the presentation of endogenous viral antigens on MHC class I molecules during HSV-1 infection [J].
English, Luc ;
Chemali, Magali ;
Duron, Johanne ;
Rondeau, Christiane ;
Laplante, Annie ;
Gingras, Diane ;
Alexander, Diane ;
Leib, David ;
Norbury, Christopher ;
Lippe, Roger ;
Desjardins, Michel .
NATURE IMMUNOLOGY, 2009, 10 (05) :480-487
[22]   Autophagy is involved in T cell death after binding of HIV-1 envelope proteins to CXCR4 [J].
Espert, Lucile ;
Denizot, Melanie ;
Grimaldi, Marina ;
Robert-Hebmann, Veronique ;
Gay, Bernard ;
Varbanov, Mihayl ;
Codogno, Patrice ;
Biard-Piechaczyk, Martine .
JOURNAL OF CLINICAL INVESTIGATION, 2006, 116 (08) :2161-2172
[23]   Differential Role of Autophagy in CD4 T Cells and Macrophages during X4 and R5 HIV-1 Infection [J].
Espert, Lucile ;
Varbanov, Mihayl ;
Robert-Hebmann, Veronique ;
Sagnier, Sophie ;
Robbins, Ian ;
Sanchez, Francoise ;
Lafont, Virginie ;
Biard-Piechaczyk, Martine .
PLOS ONE, 2009, 4 (06)
[24]   Ambra1 regulates autophagy and development of the nervous system [J].
Fimia, Gian Maria ;
Stoykova, Anastassia ;
Romagnoli, Alessandra ;
Giunta, Luigi ;
Di Bartolomeo, Sabrina ;
Nardacci, Roberta ;
Corazzari, Marco ;
Fuoco, Claudia ;
Ucar, Ahmet ;
Schwartz, Peter ;
Gruss, Peter ;
Piacentini, Mauro ;
Chowdhury, Kamal ;
Cecconi, Francesco .
NATURE, 2007, 447 (7148) :1121-U14
[25]   Identification of the in vivo role of a viral bcl-2 [J].
Gangappa, S ;
van Dyk, LF ;
Jewett, TJ ;
Speck, SH ;
Virgin, HW .
JOURNAL OF EXPERIMENTAL MEDICINE, 2002, 195 (07) :931-940
[26]   Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice [J].
Hara, Taichi ;
Nakamura, Kenji ;
Matsui, Makoto ;
Yamamoto, Akitsugu ;
Nakahara, Yohko ;
Suzuki-Migishima, Rika ;
Yokoyama, Minesuke ;
Mishima, Kenji ;
Saito, Ichiro ;
Okano, Hideyuki ;
Mizushima, Noboru .
NATURE, 2006, 441 (7095) :885-889
[27]   The gamma(1)34.5 protein of herpes simplex virus I complexes with protein phosphatase 1 alpha to dephosphorylate the alpha subunit of the eukaryotic translation initiation factor 2 and preclude the shutoff of protein synthesis by double-stranded RNA-activated protein kinase [J].
He, B ;
Gross, M ;
Roizman, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (03) :843-848
[28]   Nutrient-dependent mTORC1 Association with the ULK1-Atg13-FIP200 Complex Required for Autophagy [J].
Hosokawa, Nao ;
Hara, Taichi ;
Kaizuka, Takeshi ;
Kishi, Chieko ;
Takamura, Akito ;
Miura, Yutaka ;
Iemura, Shun-ichiro ;
Natsume, Tohru ;
Takehana, Kenji ;
Yamada, Naoyuki ;
Guan, Jun-Lin ;
Oshiro, Noriko ;
Mizushima, Noboru .
MOLECULAR BIOLOGY OF THE CELL, 2009, 20 (07) :1981-1991
[29]   Human cytomegalovirus infection activates and regulates the unfolded protein response [J].
Isler, JA ;
Skalet, AH ;
Alwine, JC .
JOURNAL OF VIROLOGY, 2005, 79 (11) :6890-6899
[30]   Beclin 1 Forms Two Distinct Phosphatidylinositol 3-Kinase Complexes with Mammalian Atg14 and UVRAG [J].
Itakura, Eisuke ;
Kishi, Chieko ;
Inoue, Kinji ;
Mizushima, Noboru .
MOLECULAR BIOLOGY OF THE CELL, 2008, 19 (12) :5360-5372