It is hard to make direct transcriptional comparisons between discrete cell populations; however, as blood cells appear to be a primary target for PRV replication [7] and infiltrating blood-associated cells are likely responsible for increases in Mx transcription relative to cardiac myocytes during myocarditis based on viral tropisms, it is curious as to why PRV would cause such an elevated antiviral transcriptional response in heart tissues. Here, MX1 is linked to myocarditis.