IL1B and Epstein-Barr virus infection: During the prelatent stage of primary EBV infection, EBV transiently expresses BHRF1 to promote AIM2 inflammasome activation in cooperation with viral genomic dsDNA; consequently, increased IL-1β/IL-18 secretion triggers antiviral and antitumor immune and inflammatory responses, serving as host restriction factors for the establishment of latency and persistent infection.