The mechanisms of these observed differences are unclear, but may include the following reasons: (1) sensitivity of the polymerase during treatment; (2) natural differences in the immune system’s elimination of differences in specific HBV genotypes; (3) BCP (basal core promoter) mutations in HBV genotypes A and C are often higher than those in D and B genotypes, while BCP mutations are associated with promoting viral replication, poor response to treatment and advanced liver disease [26, 27]. Here, OPN1SW is linked to liver disorder.