DPV UL41 gene encoding protein induces host shutoff activity and affects viral replication

•DPV pUL41 degrades RNA polymerase (Pol) II-transcribed translatable RNA and induces protein synthesis shutoff.•DPV CHv-BAC-ΔUL41 mutant virus exhibits a significant viral growth defect and plaque size reduction in DEF cells.•DPV pUL41 significantly affects the viral DNA replication and viral releas...

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Veröffentlicht in:Veterinary microbiology 2021-04, Vol.255, p.108979-108979, Article 108979
Hauptverfasser: He, Tianqiong, Wang, Mingshu, Cheng, Anchun, Yang, Qiao, Jia, Renyong, Wu, Ying, Huang, Juan, Tian, Bin, Liu, Mafeng, Chen, Shun, Zhao, Xin-Xin, Zhu, Dekang, Zhang, Shaqiu, Ou, Xuming, Mao, Sai, Gao, Qun, Sun, Di
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Sprache:eng
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Zusammenfassung:•DPV pUL41 degrades RNA polymerase (Pol) II-transcribed translatable RNA and induces protein synthesis shutoff.•DPV CHv-BAC-ΔUL41 mutant virus exhibits a significant viral growth defect and plaque size reduction in DEF cells.•DPV pUL41 significantly affects the viral DNA replication and viral release.•DPV pUL41 regulates viral mRNA accumulation. The virion host shutoff (VHS) protein, encoded by the UL41 gene of herpes simplex virus (HSV), specifically degrades mRNA and induces host shutoff. VHS and its homologs are highly conserved in the Alphaherpesvirinae subfamily. However, the role of the duck plague virus (DPV) UL41 gene is unclear. In this study, we found that the DPV UL41 gene-encoded protein (pUL41) degrades RNA polymerase (pol) II-transcribed translatable RNA and induces protein synthesis shutoff. DPV pUL41 was dispensable for viral replication, but the UL41-deleted mutant virus exhibited a significant viral growth defect and plaque size reduction in Duck embryo fibroblast (DEF) cells. Furthermore, DPV pUL41 regulated viral mRNA accumulation to affect viral DNA replication, release and cell-to-cell spread.
ISSN:0378-1135
1873-2542
DOI:10.1016/j.vetmic.2021.108979