Laodelphax Striatellusatg8 Facilitates Rice Stripe Virus Infection In An Autophagy-Independent Manner

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 striatellusis the major insect vector for RSV. In this study, we explored the interactions between RSV infection andL. striatellusautophagy, a potential intrinsic antiviral mechanism in insects. We found thatL. striatellusautophagic activity did not affect RSV infection; however, the autophagy-related-8 (Atg8) gene significantly enhanced virus infection. During RSV initial infection within theL. striatellusmidgut, silencing ofAtg8expression significantly decreased the phosphorylation of c-Jun N-terminal kinase (p-JNK); however, when RSV infection is absent, silencing of Atg8 did not alterp-JNK levels. These results indicated that Atg8 might activate the JNK machinery by allowing more virus infection into cells. We further revealed thatAtg8-deficiency significantly decreased RSV accumulation on the surface of the insect midgut epithelial cells, suggesting a receptor trafficking function of the gamma-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 thatAtg8-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 ofL. striatellusAtg8 that enhances RSV initial infection by increasing virus attachment on the infection sites.