Age-associated B cells are long-lasting effectors that impede latent γHV68 reactivation

Age-associated B cells (ABCs; CD19(+)CD11c(+)T-bet(+)) are a unique population that are increased in an array of viral infections, though their role during latent infection is largely unexplored. Here, we use murine gammaherpesvirus 68 (gamma HV68) to demonstrate that ABCs remain elevated long-term during latent infection and express IFN gamma and TNF. Using a recombinant gamma HV68 that is cleared following acute infection, we show that ABCs persist in the absence of latent virus, though their expression of IFN gamma and TNF is decreased. With a fluorescent reporter gene-expressing gamma HV68 we demonstrate that ABCs are infected with gamma HV68 at similar rates to other previously activated B cells. We find that mice without ABCs display defects in anti-viral IgG2a/c antibodies and are more susceptible to reactivation of gamma HV68 following virus challenges that typically do not break latency. Together, these results indicate that ABCs are a persistent effector subset during latent viral infection that impedes gamma HV68 reactivation.

Automated summary

ABCs, a unique subset of B cells associated with age, remain elevated and express IFN gamma and TNF during latent viral infection. They persist in the absence of latent virus but with decreased expression of IFN gamma and TNF. Mice without ABCs show defects in anti-viral antibodies and are more susceptible to reactivation of the latent virus.