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.