Prototype foamy virus elicits complete autophagy involving the ER stress-related UPR pathway.
Prototype foamy virus elicits complete autophagy involving the ER stress-related UPR pathway.
复制标题
原型泡沫病毒引发涉及内质网应激相关 UPR 途径的完全自噬
DOI：
10.1186/s12977-017-0341-x
复制
发表时间：
2017-03-07
期刊：
影响因子：
3.3
通讯作者：
Liu W
中科院分区：
文献类型：
--
作者：
Yuan P;Dong L;Cheng Q;Wang S;Li Z;Sun Y;Han S;Yin J;Peng B;He X;Liu W
BackgroundPrototype foamy virus (PFV) is a member of the Spumaretrovirinae subfamily of retroviruses, which maintains lifelong latent infection while being nonpathogenic to their natural hosts. Autophagy is a cell-programmed mechanism that plays a pivotal role in controlling homeostasis and defense against exotic pathogens. However, whether autophagy is the mechanism for host defense in PFV infection has not been investigated.FindingsOur results revealed that PFV infection induced the accumulation of autophagosomes and triggered complete autophagic flux in BHK-21 cells. PFV infection also altered endoplasmic reticulum (ER) homeostasis. The PERK, IRE1 and ATF6 pathways, all of which are components of the ER stress-related unfolded protein response (UPR), were activated in PFV-infected cells. In addition, accelerating autophagy suppressed PFV replication, and inhibition of autophagy promoted viral replication.ConclusionsOur data indicate that PFV infection can induce complete autophagy through activating the ER stress-related UPR pathway in BHK-21 cells. In turn, autophagy negatively regulates PFV replication.
