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Porcine teschovirus 2 induces an incomplete autophagic response in PK-15 cells

Gu, Yuanxing, Zhou, Yingshan, Shi, Xinfeng, Xin, Yongping, Shan, Ying, Chen, Cong, Cao, Tong, Fang, Weihuan, Li, Xiaoliang
Archives of virology 2018 v.163 no.3 pp. 623-632
Porcine teschovirus, autophagy, pathogens, protein degradation, rapamycin, viruses
Autophagy is a homeostatic process that has been shown to be vital in the innate immune defense against pathogens. However, little is known about the regulatory role of autophagy in porcine teschovirus 2 (PTV-2) replication. In this study, we found that PTV-2 infection induces a strong increase in GFP-LC3 punctae and endogenous LC3 lipidation. However, PTV-2 infection did not enhance autophagic protein degradation. When cellular autophagy was pharmacologically inhibited by wortmannin or 3-methyladenine, PTV-2 replication increased. The increase in virus yield via autophagy inhibition was further confirmed by silencing atg5, which is required for autophagy. Furthermore, PTV-2 replication was suppressed when autophagy was activated by rapamycin. Together, the results suggest that PTV-2 infection activates incomplete autophagy and that autophagy then inhibits further PTV-2 replication.