B cell-intrinsic IRF-1 and conserved gammaherpesvirus protein kinase cooperate to promote murine gammaherpesvirus-driven germinal center response and splenic latent reservoir.

ABSTRACT: Gammaherpesviruses infect >90% of adults and are associated with B cell lymphomas. These viruses drive the expansion and differentiation of germinal center B cells to amplify latent viral reservoir and ensure life-long infection of memory B cells. Additionally, infected germinal center B cells seed viral lymphomagenesis. We previously demonstrated that global deficiency of Interferon Regulatory Factor-1 (IRF-1), a classically antiviral transcription factor, results in increased murine gammaherpesvirus-driven germinal center response and latent viral reservoir. In contrast, B cell-specific loss of IRF-1 expression attenuates murine gammaherpesvirus chronic infection and germinal center response. All gammaherpesviruses encode a conserved protein kinase. We previously showed that the murine g

SUBMITTER: Rahlf CR 

PROVIDER: S-EPMC12724244 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature