Edward S. Dornan

TL;DR: The results suggest that HBIG after OLT imposes a selection pressure on the S‐gene, and that mutations are one mechanism for reinfection while receiving H BIG.

TL;DR: It is shown that the E5-induced reduction of HLA-A2 has a functional impact by reducing recognition of E5 expressing cells by HPV specific CD8+ T cells.

TL;DR: An ineffective anti-HBc B cell response accounts for ongoing disease and selection of mutations after seroconversion, in those who remit, mutations in the major T helper epitope allow immune escape, thus minimizing immune-mediated hepatitis.

TL;DR: Overall, the results suggest that interactions between TopBP1 and E2 and between Brd4 and E1 are required to correctly initiate DNA replication but are not required for continuing DNA replication, which may be mediated by alternative processes such as rolling circle amplification and/or homologous recombination.

TL;DR: The generation of an HPV16 E2 mutant compromised in TopBP1 interaction in vivo is reported and it is demonstrated that this mutant retains transcriptional activation and repression functions but has suboptimal DNA replication potential, presenting a potential new antiviral target, the E2-Top BP1 interaction, and increasing understanding of the viral life cycle.