In order to analyze whether the potency of PKR inhibition by VACV and CMLV K3 orthologs correlates with the ability of these proteins to support productive infection, we cloned VACV K3L and CMLV 032 into the E3L locus of the highly attenuated VACV strain VC-R4, which lacks both K3L and E3L and can only replicate in the absence of PKR or in cells that express exogenous PKR inhibitors [24]. The gene discussed is EIF2AK2; the disease is infection.