Casein kinase 1α(CK1α) mediates the phosphorylation and degradation of interferon-α/β receptor 1(IFNAR1) in response to viral infection. However, how CK1α regulates hepatitis B virus(HBV) replication and the anti...Casein kinase 1α(CK1α) mediates the phosphorylation and degradation of interferon-α/β receptor 1(IFNAR1) in response to viral infection. However, how CK1α regulates hepatitis B virus(HBV) replication and the anti-HBV effects of IFN-α are less reported. Here we show that CK1α can interact with IFNAR1 in hepatoma carcinoma cells and increased the abundance of IFNAR1 by reducing the ubiquitination levels in the presence of HBV.Furthermore, CK1α promotes the IFN-α triggered JAK-STAT signaling pathway and consequently enhances the antiviral effects of IFN-α against HBV replication. Our results collectively provide evidence that CK1α positively regulates the anti-HBV activity of IFN-α in hepatoma carcinoma cells, which would be a promising therapeutic target to improve the effectiveness of IFN-α therapy to cure CHB.展开更多
基金supported by the National Key Research and Development Program of China(2018YFE0107500)the Natural Science Foundation Project of Science and Technology Agency of Chongqing YuZhong District(20200122)to Hu Yuana Natural Science Foundation Project of CQ CSTC(cstc2021jcyj-msxmX0276)to Chen YanMeng
文摘Casein kinase 1α(CK1α) mediates the phosphorylation and degradation of interferon-α/β receptor 1(IFNAR1) in response to viral infection. However, how CK1α regulates hepatitis B virus(HBV) replication and the anti-HBV effects of IFN-α are less reported. Here we show that CK1α can interact with IFNAR1 in hepatoma carcinoma cells and increased the abundance of IFNAR1 by reducing the ubiquitination levels in the presence of HBV.Furthermore, CK1α promotes the IFN-α triggered JAK-STAT signaling pathway and consequently enhances the antiviral effects of IFN-α against HBV replication. Our results collectively provide evidence that CK1α positively regulates the anti-HBV activity of IFN-α in hepatoma carcinoma cells, which would be a promising therapeutic target to improve the effectiveness of IFN-α therapy to cure CHB.
