How a common virus's hijack of cell repair processes may promote cancer
Most people will become infected with Epstein-Barr virus, or EBV, at some point in their lives. In addition to being a common herpesvirus, EBV persists in its host for life as a "quiet" or latent infection. While EBV infection may have no symptoms, it often causes mild illnesses such as mononucleosis (known as the "kissing disease," because EBV spreads through saliva). In rarer instances, EBV…
When the Epstein-Barr virus becomes active again during a stage known as the lytic phase, it hijacks the host cell's DNA repair mechanisms to replicate itself. This process generates widespread DNA damage, which should typically cause the cell to stop functioning. However, the virus has developed a strategy to keep the host cell alive long enough to complete its replication cycle.
A new study published in the Proceedings of the National Academy of Sciences explores how this happens. By analyzing over 850,000 infected B cells, researchers found that while the DNA damage response is initiated, it is interrupted later on in the process. This disruption could potentially lead to genomic instability, making the infected cells more prone to developing cancer.
The findings suggest that understanding this link could provide valuable insights into how EBV-associated cancers may develop.
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