During the normal course of an infection, the virus traffics from the site of lytic replication in the lung to the draining lymph nodes and spleen where latency is established. We reasoned that the decreased frequency of latently infected splenocytes during MHV68.DHS infection could be a consequence of a defect in trafficking, persistence at these sites, or a latency establishment defect. We quantified levels of virus in the cervical lymph node at 10 dpi, an intermediate time point after peak virus replication in the lung but before peak latency establishment in the spleen. Following an intranasal inoculation, high levels of MHV68 have been found in the cervical lymph node at this time point [30, 32] . Interestingly, we detected significantly lower levels of MHV68.DHS at this site relative to MHV68.MR ( Figure 8A ), suggesting that muSOX-induced mRNA degradation contributes to the ability of the virus to traffic to or persist at the sites of latency establishment.