Robert E. White

TL;DR: It is proposed that heightened oncogenic activity in early cell divisions activates a growth-suppressive DDR which is attenuated by viral latency products to induce cell immortalization.

TL;DR: This work uses rapid, cost-effective sequencing to determine 71 new EBV sequences from different sample types and locations worldwide, and gives the first overview of EBV genome variation, important for designing vaccines and immune therapy for EBV, and provides techniques to investigate relationships between viral sequence variation and EBV-associated diseases.

TL;DR: Rec recombinant EBVs from which each of the EBNA3 genes has been independently deleted, and revertant viruses in which the genes have been re-introduced into the viral genome are created to explain the selection pressure that gives rise to a subset of BL that retain expression of theEBNA3 proteins.

TL;DR: It is concluded that latent EBV initiates a chain of events that leads to epigenetic repression of the tumour suppressor gene Bim in infected B cells and their progeny and this reprogramming of B cells could have important implications for the understanding of EBV persistence and the pathogenesis ofEBV-associated disease, in particular BL.

TL;DR: EBNA3B is a virus-encoded tumor suppressor whose inactivation promotes immune evasion and virus-driven lymphomagenesis in NOD/SCID/γc-/- mice with reconstituted human immune system components.