Both UV-inactivated and heat-inactivated influenza A viruses are more potent than wild-type viruses in inducing the production of type I interferon [16] . Cytopathogenecity has been associated with translational shut-down of host genes including interferon [44] . PRRSV is highly pathogenic in alveolar macrophages and monocyte-derived dendritic cells and rapidly destroys these target cells by apoptosis and necrosis [2, 45, 46] . Studies have clearly shown that interferon mRNA has a short life span after induction [43, 47] . We speculate that the combination of high cytopathogenicity of virus and short half-life of interferon mRNAs may at least partially contribute to the low interferon proteins detected in virus-infected cells. It is also possible that the variability of different PRRSV isolates in inducing type I interferon is related to their varied cytopathogenicity [20, 23, 48] . For influenza A virus, different isolates can vary in their ability to induce interferon by up to 100-fold [16] . Finally, it remains to be determined whether PRRSV induces the shutoff of host protein synthesis to favor its own protein synthesis. More research efforts should be directed to the understanding of the translational control of type I interferon by PRRSV in its natural host cells.