FIG 7.

Working model. (A) ATM regulates the establishment of viral latency indirectly by promoting B cell differentiation, including MHV68-driven germinal center reaction, class switching, and efficient generation of plasma B cells. These plasma cells, when derived from MHV68-infected germinal center B cells, mediate MHV68 reactivation, producing infectious virus that reseeds the B cell compartment. Suboptimal differentiation of ATM-deficient B cells indirectly attenuates the establishment of peak MHV68 latent reservoir and reactivation. (B) ATM expression by peritoneal B cells likely directly facilitates MHV68 reactivation during long-term infection.