HBV inhibits the level of endogenous interferon and induces SOCS1 and SOCS3 expression; however, following interferon treatment, HBV replication is inhibited, and the expression levels of SOCS1 and SOCS3 begin to decrease, indicating that HBV may achieve sustained infection in vivo by upregulating the expression of the SOCS proteins [68]. This evidence concerns the gene SOCS1 and infection.