Dual defects in HBsAg antigenicity and secretion caused by the C138R mutation in the S gene trigger occult hepatitis B virus infection

The C138R mutation contributed to OBI by simultaneously impairing HBsAg antigenicity and secretion. Disruption of the disulfide bond between aa107 and aa138, resulting in the formation of structurally abnormal dimers, represented the primary mechanism underlying HBsAg dysfunction caused by this mutation.