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Gammaherpesviruses such as Epstein-Barr virus (EBV), Kaposi’s sarcoma-associated virus (KSHV), and murine gammaherpesvirus 68 (MHV68) establish latent infection in B cells, macrophages, and nonlymphoid cells and can induce both lymphoid and nonlymphoid cancers. Research on these viruses has relied heavily on immortalized B cell and endothelial cell lines. Therefore, we know very little about the cell type-specific regulation of virus infection. We have previously shown that treatment of MHV68-infected macrophages with the cytokine interleukin-4 (IL-4) or challenge of MHV68-infected mice with an IL-4-inducing parasite leads to virus reactivation. However, we do not know if all latent reservoirs of the virus, including B cells, reactivate the virus in response to IL-4. Here, we used an in vivo approach to address the question of whether all latently infected cell types reactivate MHV68 in response to a …