Infectious Bursal Disease Virus Subverts Autophagic Vacuoles To Promote Viral Maturation and Release

文献类型： 外文期刊

第一作者： Wang, Yongqiang

作者： Wang, Yongqiang;Duan, Yulu;Han, Chunyan;Yao, Shuai;Qi, Xiaole;Gao, Yulong;Zhang, Lizhou;Gao, Li;Gao, Honglei;Shen, Nan;Wang, Jingfei;Wang, Xiaomei;Maier, Helena J.;Britton, Paul;Chen, Lei

作者机构：

关键词： IBDV;autophagy;maturation;release

期刊名称：JOURNAL OF VIROLOGY （ 影响因子：5.103； 五年影响因子：5.078 ）

ISSN：

年卷期：

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收录情况： SCI

摘要： Autophagy functions as an intrinsic antiviral defense. However, some viruses can subvert or even enhance host autophagic machinery to increase viral replication and pathogenesis. The role of autophagy during avibirnavirus infection, especially late stage infection, remains unclear. In this study, infectious bursal disease virus (IBDV) was used to investigate the role of autophagy in avibirnavirus replication. We demonstrated IBDV induction of autophagy as a significant increase in puncta of LC3-I autophagosomes, endogenous levels of LC3-II, and ultrastructural characteristics typical of autophagosomes during the late stage of infection. Induction of autophagy enhances IBDV replication, whereas inhibition of autophagy impairs viral replication. We also demonstrated that IBDV infection induced autophagosome-lysosome fusion, but without active degradation of their contents. Moreover, inhibition of fusion or of lysosomal hydrolysis activity significantly reduced viral replication, indicating that virions utilized the low-pH environment of acidic organelles to facilitate viral maturation. Using immuno-transmission electron microscopy (TEM), we observed that a large number of intact IBDV virions were arranged in a lattice surrounded by p62 proteins, some of which lay between virions. Additionally, many virions were encapsulated within the vesicular membranes, with an obvious release stage observed by TEM. The autophagic endosomal pathway facilitates low-pH-mediated maturation of viral proteins and membrane-mediated release of progeny virions.

分类号： Q934.2

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