Figure 1.

EBV’s impact on apoptosis inhibition and the stimulation of infected cell proliferation. Apoptosis inhibition primarily occurs via two mechanisms (1): Latency proteins LMP1 and LMP2 modulate various molecules and transcriptional pathways, suppressing host cell apoptosis to facilitate EBV latency persistence; and (2) Infection in nasopharyngeal epithelial cells prompts LMP1 accumulation and p53 phosphorylation, inhibiting apoptosis. Additionally, cell proliferation and B cell survival are predominantly induced by (1): EBER1 enhances mitochondrial activity and calcium influx; and (2) LMP1 induces different transcription factors associated with promoting cell proliferation and B cell survival. EBV miRNAs, particularly miR-BART20-5p and miR-BART11-5p, play a pivotal role in both inhibiting apoptosis and promoting cell proliferation.