Infectious bursal disease virus (IBDV) is an important immunosuppressive virus of chickens. Although the gene functions of IBDV have been well characterized, the host responses during IBDV infection remain much poor. In the present study, casein kinase 1 alpha (CK1α), a novel VP2-associated protein, was down-regulated during IBDV replication in DF1 cells. Further experiments showed that siRNA-mediated knockdown of CK1α inhibited IBDV replication, while overexpression of CK1α promoted IBDV growth. Finally, we revealed that the effects of CK1α expression level on IBDV replication were involved in the negative regulation of CK1α on type I interferon receptor (IFNAR1), because ubiquitination assay analyses demonstrated that CK1α could promote the ubiquitination of IFNAR1, thereby affecting the stability of this receptor. In conclusion, down-regulation of CK1α during IBDV infection as a host defense response increased abundance of IFNAR1, which in turn enhanced an inhibitory effect on IBDV replication.

传染性法氏囊病病毒（IBDV）是一种重要的鸡免疫抑制病毒。尽管已经很好地表征了IBDV的基因功能，但是IBDV感染期间的宿主反应仍然很差。在本研究中，酪蛋白激酶1α（CK1α），一种新型的VP2相关蛋白，在DF1细胞中IBDV复制过程中被下调。进一步的实验表明，siRNA介导的CK1α的敲低抑制了IBDV复制，而CK1α的过表达促进了IBDV的生长。最后，我们发现CK1α表达水平对IBDV复制的影响与CK1α对I型干扰素受体（IFNAR1）的负调控有关，因为泛素化分析表明CK1α可以促进IFNAR1的泛素化，从而影响IFNAR1的稳定性。这个受体。综上所述，