KRT88P and infection: However, HBV-HBc-AAP infection of Par14- or Par17-overexpressing HepG2-hNTCP-C9 cells did not affect HBV replication at all (Figure 8C, lanes 5 vs. 6 and 7), demonstrating that the RP motif of HBc is critical for Par14/Par17-mediated upregulation of HBV replication.