B cell-intrinsic STAT3-mediated support of latency and interferon suppression during murine gammaherpesvirus 68 infection revealed through an in vivo competition model.

ABSTRACT: Cancers associated with the oncogenic gammaherpesviruses, Epstein-Barr virus and Kaposi sarcoma herpesvirus, are notable for their constitutive activation of the transcription factor STAT3. To better understand the role of STAT3 during gammaherpesvirus latency and immune control, we utilized murine gammaherpesvirus 68 (MHV68) infection. Genetic deletion of STAT3 in B cells of CD19^cre/+Stat3^f/f mice reduced peak latency approximately 7-fold. However, infected CD19^cre/+Stat3^f/f mice exhibited disordered germinal centers and heightened virus-specific CD8 T cell responses compared to WT littermates. To circumvent the systemic immune alterations observed in the B cell-STAT3 knockout mice and more

SUBMITTER: Hogan CH 

PROVIDER: S-EPMC10055336 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature