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Open AccessCommunication

Seneca Valley Virus 3Cpro Cleaves PABPC1 to Promote Viral Replication

State Key Laboratory of Veterinary Etiological Biology, National Foot and Mouth Diseases Reference Laboratory, Key Laboratory of Animal Virology of Ministry of Agriculture, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, China
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Pathogens 2020, 9(6), 443; https://doi.org/10.3390/pathogens9060443
Received: 4 May 2020 / Revised: 1 June 2020 / Accepted: 2 June 2020 / Published: 4 June 2020
(This article belongs to the Section Animal Pathogens)
Seneca Valley Virus (SVV) is an oncolytic virus of the Picornaviridae family, which has emerged in recent years. The impact of SVV on host cell translation remains unknown. Here, we showed, for the first time, that SVV infection cleaved poly(A) binding protein cytoplasmic 1 (PABPC1). In SVV-infected cells, 50 kDa of the N terminal cleaved band and 25 kDa of the C terminal cleaved band of PABPC1 were detected. Further study showed that the viral protease, 3Cpro induced the cleavage of PABPC1 by its protease activity. The SVV strains with inactive point mutants of 3Cpro (H48A, C160A or H48A/C160A) can not be rescued by reverse genetics, suggesting that sites 48 and 160 of 3Cpro were essential for SVV replication. SVV 3Cpro induced the cleavage of PABPC1 at residue 437. A detailed data analysis showed that SVV infection and the overexpression of 3Cpro decreased the protein synthesis rates. The protease activity of 3Cpro was essential for inhibiting the protein synthesis. Our results also indicated that PABPC1 inhibited SVV replication. These data reveal a novel antagonistic mechanism and pathogenesis mediated by SVV and highlight the importance of 3Cpro on SVV replication. View Full-Text
Keywords: seneca valley virus; 3Cpro; antagonistic mechanism; PABPC1; translation seneca valley virus; 3Cpro; antagonistic mechanism; PABPC1; translation
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MDPI and ACS Style

Xue, Q.; Liu, H.; Zhu, Z.; Xue, Z.; Liu, X.; Zheng, H. Seneca Valley Virus 3Cpro Cleaves PABPC1 to Promote Viral Replication. Pathogens 2020, 9, 443.

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