Chen Yong, Chen Qian, Li Manman, Mao Qianzhuo, Chen Hongyan, Wu Wei, Jia Dongsheng, Wei Taiyun
Fujian Province Key Laboratory of Plant Virology, Institute of Plant Virology, Fujian Agriculture and Forestry University, Fuzhou, Fujian, PR China.
Fujian Key Laboratory for Monitoring and Integrated Management of Crop Pests, Institute of Plant Protection, Fujian Academy of Agricultural Sciences, Fuzhou, Fujian, PR China.
PLoS Pathog. 2017 Nov 10;13(11):e1006727. doi: 10.1371/journal.ppat.1006727. eCollection 2017 Nov.
Many viral pathogens are persistently transmitted by insect vectors and cause agricultural or health problems. Generally, an insect vector can use autophagy as an intrinsic antiviral defense mechanism against viral infection. Whether viruses can evolve to exploit autophagy to promote their transmission by insect vectors is still unknown. Here, we show that the autophagic process is triggered by the persistent replication of a plant reovirus, rice gall dwarf virus (RGDV) in cultured leafhopper vector cells and in intact insects, as demonstrated by the appearance of obvious virus-containing double-membrane autophagosomes, conversion of ATG8-I to ATG8-II and increased level of autophagic flux. Such virus-containing autophagosomes seem able to mediate nonlytic viral release from cultured cells or facilitate viral spread in the leafhopper intestine. Applying the autophagy inhibitor 3-methyladenine or silencing the expression of Atg5 significantly decrease viral spread in vitro and in vivo, whereas applying the autophagy inducer rapamycin or silencing the expression of Torc1 facilitate such viral spread. Furthermore, we find that activation of autophagy facilitates efficient viral transmission, whereas inhibiting autophagy blocks viral transmission by its insect vector. Together, these results indicate a plant virus can induce the formation of autophagosomes for carrying virions, thus facilitating viral spread and transmission by its insect vector. We believe that such a role for virus-induced autophagy is common for vector-borne persistent viruses during their transmission by insect vectors.
许多病毒病原体通过昆虫媒介持续传播，并引发农业或健康问题。一般来说，昆虫媒介可以利用自噬作为抵御病毒感染的内在抗病毒防御机制。病毒是否能够进化以利用自噬来促进其通过昆虫媒介传播仍不清楚。在此，我们表明，植物呼肠孤病毒水稻瘤矮病毒（RGDV）在培养的叶蝉媒介细胞和完整昆虫中的持续复制会触发自噬过程，这表现为明显的含病毒双膜自噬体的出现、ATG8-I 向 ATG8-II 的转化以及自噬通量水平的增加。这种含病毒的自噬体似乎能够介导病毒从培养细胞中进行非裂解性释放，或促进病毒在叶蝉肠道中的传播。应用自噬抑制剂 3-甲基腺嘌呤或沉默 Atg5 的表达可显著降低病毒在体外和体内的传播，而应用自噬诱导剂雷帕霉素或沉默 Torc1 的表达则促进这种病毒传播。此外，我们发现自噬的激活促进了病毒的有效传播，而抑制自噬则通过其昆虫媒介阻断了病毒传播。总之，这些结果表明一种植物病毒可以诱导形成携带病毒粒子的自噬体，从而促进病毒通过其昆虫媒介传播。我们认为，病毒诱导的自噬在媒介传播的持续性病毒通过昆虫媒介传播过程中具有这种作用是常见的。
