Porcine teschovirus 2 induces an incomplete autophagic response in PK-15 cells
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.
This work is partly supported by the important agriculture subject fund from Department of S&T of Zhejiang Province (2015C02044), Department of Education of Zhejiang Province (Y201635576), the Agricultural Technology Extension Funds of Zhejiang University, Dabei Agricultural Discipline Development and Talent Training Fund (2017ZDNT004), and three rural six party funds for Xiaoliang Li.
Compliance with ethical standards
Conflicts of interest
The authors declare no conflicts of interest.
All animal studies were approved by the Animal Care and Use Committee of Zhejiang University in accordance with the Chinese guidelines for the care and use of laboratory animals (Permit Number: 2016101098).
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