Epstein-Barr virus may drive cancer by exploiting DNA repair
Research on Epstein-Barr virus reveals how the pathogen uses the host cell's DNA repair system to replicate during its lytic phase. This process causes widespread damage to host DNA, and the virus must prevent infected B cells from dying so it can finish replicating. By mapping more than 850,000 infected memory B cells, scientists identified stages that may help explain EBV's role in some cancers.
Epstein-Barr virus is widespread; after initial infection it remains latent for life. While often asymptomatic or causing mononucleosis, it is linked in rare cases to multiple sclerosis and almost 2% of cancers. During reactivation, its lytic phase, EBV commandeers host DNA repair machinery to copy itself, inflicting extensive damage on cellular DNA.
To survive this, the virus must stop infected memory B cells from dying. Researchers fixed such cells at various lytic stages, built an atlas exceeding 850,000 cells, and used single-cell imaging plus pseudotime analysis. They found cells initiate DNA damage responses but fail to complete them, potentially destabilizing the genome and setting the stage for malignancy.
Because EBV is nearly ubiquitous, these findings could eventually shape how clinicians consider viral reactivation and cancer risk, especially for people with EBV-linked cancers or multiple sclerosis. Mapping lytic stages may guide future research into mechanisms, yet any clinical benefit—such as risk assessment or targeted treatment—remains uncertain and likely years away.