Henri Gruffat

TL;DR: The EBV genome codes for several transcriptional trans-activators, such as BZLF1 open reading frame (ORF)-encoded product EB1, which is able to induce the productive cycle in infected B cells as mentioned in this paper.

TL;DR: It is shown that R, produced either by in vitro translation, or present in nuclear extracts from HeLa cells constitutively producing R, binds directly to and protects against DNAase I digestion, two regions in RRE-DR.

TL;DR: Evidence is presented that, during latency, proteins of the myocyte enhancer binding factor 2 (MEF2) family are bound to the BZLF1 promoter and recruit class II histone deacetylases, and it is proposed that latency is determined primarily by a specific and local recruitment of class II Histone de acetylase (HDAC) by MEF2D to theBZLf1 gene promoter.

TL;DR: It is shown that EBV can alter the regulation and expression of TLRs, the key effector molecules of the innate immune response, and that the EBV oncoprotein latent membrane protein 1 (LMP1) is a strong inhibitor of TLR9 transcription.

TL;DR: It is shown that EB2 is necessary for the production of infectious EBV and that its function cannot be transcomplemented by a cellular factor, and two herpesvirus homologs of the EB2 protein, the herpes simplex virus type 1 protein ICP27 and the human cytomegalovirus protein UL69, only partly rescued the phenotype of theEBVBMLF1-KO mutant.