期刊
EBIOMEDICINE
卷 1, 期 2-3, 页码 116-125出版社
ELSEVIER
DOI: 10.1016/j.ebiom.2014.11.007
关键词
Atg8/LC3; Atg12; Atg16; BZLF1; Lytic EBV replication; Epithelial cell; B cell
资金
- Cancer Research Switzerland [KFS-3234-08-2013]
- Association for International Cancer Research [11-0516, 14-1033]
- KFSPMS and KFSPHLD of the University of Zurich
- Baugarten Foundation
- Sobek Foundation
- Fondation Acteria
- Wellcome Trust
- Leukaemia and Lymphoma Research
- Medical Research Council
- Swiss National Science Foundation [310030_143979, CRSII3_136241]
- Swiss National Science Foundation (SNF) [310030_143979] Funding Source: Swiss National Science Foundation (SNF)
Epstein Barr virus (EBV) persists as a latent herpes virus infection in the majority of the adult human population. The virus can reactivate from this latent infection into lytic replication for virus particle production. Here, we report that autophagic membranes, which engulf cytoplasmic constituents during macroautophagy and transport them to lysosomal degradation, are stabilized by lytic EBV replication in infected epithelial and B cells. Inhibition of autophagic membrane formation compromises infectious particle production and leads to the accumulation of viral DNA in the cytosol. Vice versa, pharmacological stimulation of autophagic membrane formation enhances infectious virus production. Atg8/LC3, an essential macroautophagy protein and substrate anchor on autophagic membranes, was found in virus preparations, suggesting that EBV recruits Atg8/LC3 coupled membranes to its envelope in the cytosol. Our data indicate that EBV subverts macroautophagy and uses autophagic membranes for efficient envelope acquisition during lytic infection. (C) 2014 The Authors. Published by Elsevier B.V.
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