All herpesviruses exhibit a biphasic lifecycle. In the latent state few viral genes are expressed, and the viral genome is maintained in the nucleus of the host cell until stimulating signals induce lytic reactivation [12, 13, 14] . Most gammaherpesvirus-induced diseases are associated with latency. During the lytic cycle the vast majority of viral genes are expressed, and the virus undergoes active replication to produce progeny virions. At this stage during productive replication, gammaherpesviruses induce global mRNA degradation via the product of the alkaline exonuclease gene, termed SOX in KSHV, muSOX (ORF37) in MHV68, and BGLF5 in EBV [1, 15, 16] . SOX and its homologs are conserved in all subfamilies of herpesviruses, where they were first identified as DNA exonucleases critical for the resolution of branched structures that arise during viral DNA replication [17, 18, 19, 20] .