Zhang L(1), Li H(1), Chen Y(1), Gao X(1), Lu Z(1), Gao L(1), Wang Y(1), Gao Y(1),Gao H(1), Liu C(1), Cui H(1), Zhang Y(1), Pan Q(1), Qi X(2), Wang X(3).Virology. 2017 Oct 4;512:211-221. doi: 10.1016/j.virol.2017.08.007.

Abstract

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.