The E3 ligase TRIM56 is a host restriction factor of Zika virus and depends on its RNA-binding activity but not miRNA regulation, for antiviral function

Yang, Darong; Li, Nan L.; Wei, Dahai; Liu, Baoming; Guo, Fang; Elbahesh, Husni; Zhang, Yunzhi; Zhou, Zhi; Chen, Guo-Yun; Li, Kui

To determine if endogenous TRIM56 expression restricts ZIKV in neural cells, we performed shRNA knockdown experiments in the human fetal astrocyte cell line SVGA, which expressed readily detectable TRIM56 protein. In comparison with a non-targeting control shRNA, TRIM56 shRNA significant decreased TRIM56 protein abundance (Fig 8C, compare lanes 2 vs 1) . Upon infection by ZIKV, intracellular viral E and NS5 proteins accumulated to higher levels in TRIM56 knockdown SVGA cells than in cells bearing control shRNA (Fig 8C, compare lanes 4 vs 3, and 6 vs 5) . Consistent with the immunoblotting data, TRIM56 depletion led to increased percentage of viral E protein-positive cells (Fig 8D) , heightened intracellular viral RNA replication (Fig 8E) , and elevated progeny virus production (Fig 8F) . Taken together, the data gleaned from SK-N-SH and SVGA cells demonstrate that TRIM56 also functions in human cells of neural origin to impede ZIKV replication.