Abstract
Epstein-Barr virus (EBV) remains dormant in host B cells for a long time, and more than 90% of patients are asymptomatically infected. However, some internal factors (such as immune deficiency) or exogenous factors (such as HIV infection, inflammation and hypoxia) can destroy this underlying property and lead to disease development. EBV was originally discovered in association with Burkitt lymphomas and is now etiologically associated with malignant lymphomas of B, T, and NK cell origins. Previous relevant studies have reported that EBV could promote the occurrence and development of lymphomas and affect the prognosis. In fact, the pathogenesis of EBV-associated lymphomas involves different viral gene expression patterns and complex cytogenetic changes. Here, the present study summarizes viral two life cycles, latent modes, the establishment of latency and viral reactivation. We also focus on the occurrence of EBV-related lymphomas, generalize and put forward novel perspectives or innovative solutions for treatments according to these pathogenic mechanisms.