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Host Interferon-Stimulated Gene 20 Inhibits Pseudorabies Virus Proliferation

  • Research Article
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Virologica Sinica

Abstract

Host interferon-stimulated gene 20 (ISG20) exerts antiviral effects on viruses by degrading viral RNA or by enhancing IFN signaling. Here, we examined the role of ISG20 during pseudorabies virus (PRV) proliferation. We found that ISG20 modulates PRV replication by enhancing IFN signaling. Further, ISG20 expression was upregulated following PRV infection and poly(I:C) treatment. Ectopic expression of ISG20 inhibited PRV proliferation in PK15 cells, whereas knockdown of ISG20 promoted PRV proliferation. In addition, ISG20 expression upregulated IFN-β expression and enhanced IFN downstream signaling during PRV infection. Notably, PRV UL24 suppressed the transcription of ISG20, thus antagonizing its antiviral effect. Further domain mapping analysis showed that the N terminus (amino acids 1–90) of UL24 was responsible for the inhibition of ISG20 transcription. Collectively, these findings characterize the role of ISG20 in suppressing PRV replication and increase the understanding of host-PRV interplay.

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Acknowledgements

We acknowledge the supports from the National Key Research and Development Program of China (2016YFD0500100), Shanghai Science and Technology Innovation Action Plan (17391901900), and Shanghai Municipal Agriculture Science and Technology Key Project (2016, 4-2).

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XC and GT conceived and designed the experiments; XC, DS, SD, and HZ performed the experiments. NK, HZ, WT, and GL analyzed the data; XC wrote the manuscript and prepared the figures; XC, TS, and GT checked and finalized the manuscript. All authors contributed to the article and approved the submitted version.

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Correspondence to Tongling Shan or Guangzhi Tong.

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The authors declare no conflict of interest.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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Chen, X., Sun, D., Dong, S. et al. Host Interferon-Stimulated Gene 20 Inhibits Pseudorabies Virus Proliferation. Virol. Sin. 36, 1027–1035 (2021). https://doi.org/10.1007/s12250-021-00380-0

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  • DOI: https://doi.org/10.1007/s12250-021-00380-0

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