State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Science, Beijing, China.
CAS Center for Excellence in Biotic Interactions, University of the Chinese Academy of Sciences, Beijing, China.
Insect Sci. 2021 Apr;28(2):315-329. doi: 10.1111/1744-7917.12771. Epub 2020 Jul 24.
Rice stripe virus (RSV) is the causative agent of rice stripe disease and is completely dependent on insect vectors for its plant-to-plant transmission. Laodelphax striatellus is the major insect vector for RSV. In this study, we explored the interactions between RSV infection and L. striatellus autophagy, a potential intrinsic antiviral mechanism in insects. We found that L. striatellus autophagic activity did not affect RSV infection; however, the autophagy-related-8 (Atg8) gene significantly enhanced virus infection. During RSV initial infection within the L. striatellus midgut, silencing of Atg8 expression significantly decreased the phosphorylation of c-Jun N-terminal kinase (p-JNK); however, when RSV infection is absent, silencing of Atg8 did not alter p-JNK levels. These results indicated that Atg8 might activate the JNK machinery by allowing more virus infection into cells. We further revealed that Atg8-deficiency significantly decreased RSV accumulation on the surface of the insect midgut epithelial cells, suggesting a receptor trafficking function of the γ-aminobutyric acid receptor-associated protein family. Using the RSV ovary entry as a model, in which vitellogenin receptor (VgR) mediates RSV cell entry, we clarified that Atg8-deficiency decreased the abundance of VgR localizing on the cytomembrane and disturbed the attachment of RSV in the germarium zones. Collectively, these results revealed an autophagy-independent function of L. striatellus Atg8 that enhances RSV initial infection by increasing virus attachment on the infection sites.
水稻条纹病毒（RSV）是水稻条纹病的病原体，其在植物间的传播完全依赖于昆虫媒介。褐飞虱是 RSV 的主要昆虫媒介。在这项研究中，我们探讨了 RSV 感染与褐飞虱自噬之间的相互作用，自噬是昆虫体内一种潜在的固有抗病毒机制。我们发现，褐飞虱自噬活性不会影响 RSV 感染；然而，自噬相关基因 8（Atg8）显著增强了病毒感染。在 RSV 最初感染褐飞虱中肠期间，沉默 Atg8 表达显著降低了 c-Jun N-末端激酶（p-JNK）的磷酸化；然而，当 RSV 感染不存在时，沉默 Atg8 不会改变 p-JNK 水平。这些结果表明，Atg8 可能通过允许更多的病毒感染进入细胞来激活 JNK 机制。我们进一步揭示，Atg8 缺陷显著降低了 RSV 在昆虫中肠上皮细胞表面的积累，表明 γ-氨基丁酸受体相关蛋白家族具有受体运输功能。使用 RSV 卵巢进入作为模型，其中卵黄蛋白原受体（VgR）介导 RSV 细胞进入，我们阐明了 Atg8 缺陷降低了定位于细胞质膜上的 VgR 的丰度，并扰乱了 RSV 在生殖区的附着。总的来说，这些结果揭示了褐飞虱 Atg8 的一种自噬非依赖性功能，通过增加感染部位的病毒附着来增强 RSV 的初始感染。
