Journal
VIROLOGY
Volume 559, Issue -, Pages 46-56Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2021.03.015
Keywords
Porcine deltacoronavirus; Nonstructural protein 10 (nsp10); Zinc finger; Interferon production
Categories
Funding
- National Natural Science Foundation of China [31730095, 31902247]
- National Key RD Plan of China [2016YFD0500103]
- China Postdoctoral Science Foundation [2018M640717, 2019T120670]
- Major S&T Project of Hubei Province [2017ABA138]
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The study demonstrates that PDCoV nsp10 antagonizes IFN through a ZF-independent mechanism and has a synergistic effect with nsp14 and nsp16 in inhibiting IFN-beta production.
Porcine deltacoronavirus (PDCoV) is a novel swine enteropathogenic coronavirus that causes serious vomiting and diarrhea in piglets. Previous work demonstrated that PDCoV infection inhibits type I interferon (IFN) production. Here, we found that ectopic expression of PDCoV nsp10 significantly inhibited Sendai virus (SeV)induced IFN-beta production by impairing the phosphorylation and nuclear translocation of two transcription factors, IRF3 and NF-kappa B p65 subunit. Interestingly, experiments with truncated mutants and site-directed mutagenesis revealed that PDCoV nsp10 mutants with missing or destroyed zinc fingers (ZFs) domains also impeded SeV-induced IFN-beta production, suggesting that nsp10 does not require its ZF domains to antagonize IFN beta production. Further work found that co-expression of nsp10 with nsp14 or nsp16, two replicative enzymes, significantly enhanced the inhibitory effects of nsp10 on IFN-beta. Taken together, our results demonstrate that PDCoV nsp10 antagonizes IFN via a ZF-independent mechanism and has a synergistic effect with nsp14 and nsp16 on inhibiting IFN-beta production.
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