Genetic knock out of Bmal1 and over-expression or activation of REV-ERB with synthetic agonists inhibits the replication of HCV and the related flaviruses dengue and Zika via perturbation of lipid signaling pathways.
We provide here the first report that rs4986938 in the ESR2 gene played a potential sex-specific role in the etiology of HCV infection in a high-risk Chinese Han population, suggesting that ESR2 is a candidate susceptibility gene for HCV infection and viral clearance.
At the protein level, there was a significantly higher expression of nuclear ERα in livers of HCV-related HCC patients and nuclear ERβ in HCV-related cirrhosis patients as compared to normals (<i>P</i> < 0.05).