Multifaceted roles for STAT3 in gammaherpesvirus latency revealed through in vivo B cell knockout models.

ABSTRACT: Cancers associated with the oncogenic gammaherpesviruses, Epstein-Barr virus and Kaposi sarcoma herpesvirus, are notable for their constitutive activation of the transcription factor signal transducer and activator of transcription 3 (STAT3). To better understand the role of STAT3 during gammaherpesvirus latency and the B cell response to infection, we used the model pathogen murine gammaherpesvirus 68 (MHV68). Genetic deletion of STAT3 in B cells of CD19^cre/+Stat3^f/f mice reduced peak MHV68 latency approximately sevenfold. However, infected CD19^cre/+Stat3^f/f mice exhibited disordered germinal centers and heightened virus-specific CD8 T cell responses compared to wild-type (WT) littermates. To circumvent the systemic immune alterati

SUBMITTER: Hogan CH 

PROVIDER: S-EPMC10870824 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature