2.3.1 MYC
EBV virus will initiate the transcription of MYC after infection, and also activate KC and TLR-4 pathways to maintain its own immune system, so as to escape host immune recognition and clearance, and the depletion of MYC or factors affecting MYC expression causes EBV virus to enter a lysis state. Guo Ran et al51 performed a genomic screen using CRISPR / Cas9 in Burkitt’s lymphoma B cells and identified a MYC-centered gene network in which MYC and endoglin, FACT, STAGA, and mediator collaborate to repress transcription of the BZLF1 promoter. BZLF1 primarily regulates B-cell lysis, and its transcription causes more than 30 early lytic genes, including viral DNA polymerase, the synthesis factor BMRF1, kinases and other factors important for cleaved DNA replication. The expression of Epstein-Barr nuclear antigen (EBNA), latent membrane protein (LMP), and BZLF1 was reduced after the knockdown of ubiquitin-like PHD and ring finger-containing 1 (UHRF1), DNA methyltransferase 1 (DNMT1), and polycomb repressor complex 1 (PRC1) by Guo Rui et al52. The incapability of the immune system to recognize BV virus led to a long-term latent infection in the dormitory. Sidorov et al 53 investigated the impact of IgH/c-myc translocation in primary B cells the use of CRISPR/Cas9 knock-in method and confirmed that CD4+ T cells inhibit eBL by using killing pre-eBL cells lacking IgH/c-myc translocation in vitro on the one hand; on the other hand, by means of reducing the EBNA2 expression promoter, they induced EBV transition between latencyⅢI and latency I, thereby indirectly stimulating eBL development. EBNA2 has an anti-apoptotic effect, but its loss can lead to decreased viability of the LCL. CD4+ T lymphocytes increased the expression of bcl6 mRNA in the LCL, which is an important marker of eBL.