Fig. 7

A pattern of immune escape of HBV-associated HCC tumor cells drawn by Figdraw. In HBV-associated HCC, HBV DNA polymerase inhibits the nuclear translocation of PARP1 by interacting with PARP1, thereby upregulating PD-L1 expression in tumor cells at the transcriptional level. PD-L1 on the surface of tumor cells then binds to PD-1 on the surface of T cells, which in turn inhibits T cell function and promotes HCC development