Porcine deltacoronavirus nsp10 antagonizes interferon-β production independently of its zinc finger domains

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.

Automated summary

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.