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Significance Infectious agents, including viruses, activate cellular inflammasomes. Viruses have evolved strategies to parry such host defense mechanisms, and cancer-causing gammaherpesviruses such as Epstein−Barr virus (EBV) are no exception. In distinct contrast, we show that this ubiquitous virus exploits assembly of the NLRP3 inflammasome to kick-start its lytic cascade; this allows EBV to reactivate from quiescence, propagate, and leave the cell when the cell perceives intrinsic or extrinsic threats. This discovery also provides a predictive signature that marks cells in which EBV is poised to enter the lytic phase. Importantly also, with hyperglycemia known to activate the NLRP3 inflammasome, our findings provide a mechanistic basis for recent clinical observations of diabetes as a significant risk factor for EBV-lymphomas in transplant recipients.

A promiscuous inflammasome sparks replication of a common tumor virus