The double-spliced defective variant might contribute to persistent HBV replication in a subpopulation of HCC patients.

MBP deficiency is not a significant risk factor for persistent HBV, severe malaria nor pulmonary TB in West Africa.

The ability of core 18-27-specific CD8 to tolerate epitope mutations was found only during persistent HBV infection.

Weak or absent virus-specific CD8 T-cell responses to hepatitis B virus (HBV) infection are thought to be responsible for persistent HBV infection.