We have previously shown that ISVP infection leads to the production of TGFβ, acting as a pro-survival cytokine; as such it appears that ISVP confers an infectious advantage compared to their virion counterparts by using complementary strategies (i.e. IRF3 sequestration into viral factories and production of the pro-survival factor TGFβ). The gene discussed is IRF3; the disease is infection.