To determine whether this was the root cause of the defect in latency establishment upon MHV68.DHS infection, we next infected mice via the intraperitoneal route, which bypasses the requirement for the virus to undergo acute replication and traffic through the lymph before reaching the spleen [37] . At 19 dpi, we found significantly less MHV68.DHS virus in the spleen relative to MHV68.MR by qPCR ( Figure 8B ), indicating that a defect in viral trafficking cannot fully account for the latency establishment defect observed during an intranasal infection. Collectively, these data indicate that muSOX-induced host shutoff plays important roles both in the ability of MHV68 to traffic to the lymph nodes, as well as establish latency in the spleen.