Southern rice black-streaked dwarf virus induces incomplete autophagy for persistence in gut epithelial cells of its vector insect

文献类型： 外文期刊

第一作者： Zhang, Lu

作者： Zhang, Lu;Liu, Wenwen;Wu, Nan;Wang, Hui;Wang, Xifeng;Zhang, Lu;Zhang, Zhongkai;Liu, Yule;Liu, Yule

作者机构：

期刊名称：PLOS PATHOGENS （ 影响因子：6.7； 五年影响因子：6.7 ）

ISSN： 1553-7366

年卷期： 2023 年 19 卷 1 期

页码：

收录情况： SCI

摘要： Autophagy plays an important role in virus infection of the host, because viral components and particles can be degraded by the host's autophagy and some viruses may be able to hijack and subvert autophagy for its benefit. However, details on the mechanisms that govern autophagy for immunity against viral infections or benefit viral survival remain largely unknown. Plant reoviruses such as southern rice black-streaked dwarf virus (SRBSDV), which seriously threaten crop yield, are only transmitted by vector insects. Here, we report a novel mechanism by which SRBSDV induces incomplete autophagy by blocking autophagosome-lysosome fusion, resulting in viral accumulation in gut epithelial cells of its vector, white-backed planthopper (Sogatella furcifera). SRBSDV infection leads to stimulation of the c-Jun N-terminal kinase (JNK) signaling pathway, which further activates autophagy. Mature and assembling virions were found close to the edge7 of the outer membrane of autophagosomes. Inhibition autophagy leads to the decrease of autophagosomes, which resulting in impaired maturation of virions and the decrease of virus titer, whereas activation of autophagy facilitated virus titer. Further, SRBSDV inhibited fusion of autophagosomes and lysosomes by interacting with lysosomal-associated membrane protein 1 (LAMP1) using viral P10. Thus, SRBSDV not only avoids being degrading by lysosomes, but also further hijacks these non-fusing autophagosomes for its subsistence. Our findings reveal a novel mechanism of reovirus persistence, which can explain why SRBSDV can be acquired and transmitted rapidly by its insect vector. Author summaryReoviruses can cause serious harm to mammals and cereals in the world. Understanding their persistence mechanism can contribute to control strategies. Here, we reveal that a plant reovirus, SRBSDV can activate the JNK signaling pathway through interacting with integrin beta 3 in the plasma membrane, upregulate expression of autophagy-related genes, and increase autophagosome numbers. Once inside the insect cell, SRBSDV hijacks autophagosome for accumulation, further escape degradation by inhibiting fusion between autophagosomes and lysosomes by the interaction of major outer capsid protein with LAMP1. This new mechanism explains why SRBSDV can survive in and be efficiently transmitted by a particular vector insect species and will help to design novel strategies to prevent virus transmission.

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