Sepsis erodes CD8⁺ memory T cell-protective immunity against an EBV homolog in a 2B4-dependent manner.

ABSTRACT: Epstein-Barr virus (EBV) reactivation commonly occurs following sepsis, but the mechanisms underlying this are unknown. We utilized a murine EBV homolog (gHV) and the cecal ligation and puncture model of polymicrobial sepsis to study the impact of sepsis on gHV reactivation and CD8⁺ T cell immune surveillance following a septic insult. We observed a significant increase in the frequency of gHV-infected germinal center B cells on day 7 following sepsis. This increase in viral load was associated with a concomitant significant decrease in the frequencies of gHV-specific CD8⁺ T cells, as measured by class I MHC tetramers corresponding to the immunodominant viral epitopes. Phenotypic analysis revealed an increased frequency of gHV-specific CD8⁺ T cells expressi

SUBMITTER: Xie J 

PROVIDER: S-EPMC7094871 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature