{Reference Type}: Journal Article
{Title}: Porcine deltacoronavirus nsp10 antagonizes interferon-β production independently of its zinc finger domains.
{Author}: Fang P;Hong Y;Xia S;Zhang J;Ren J;Zhou Y;Fang L;Xiao S;
{Journal}: Virology
{Volume}: 559
{Issue}: 0
{Year}: 07 2021
{Factor}: 3.513
{DOI}: 10.1016/j.virol.2021.03.015
{Abstract}: 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-β production by impairing the phosphorylation and nuclear translocation of two transcription factors, IRF3 and NF-κB 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-β production, suggesting that nsp10 does not require its ZF domains to antagonize IFN-β 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-β. 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-β production.