Once bound to their receptor on the cell surface (IFNAR), type-I IFNs activate the Janus tyrosine kinase pathway, which induces the expression of a wide spectrum of cellular genes including Pkr [18] . These different genes participate in the cellular defense against the viral infection. PKR is a serine-threonine kinase that binds dsRNA in its N-terminal regulatory region and induces phosphorylation of translation initiation factor 2-alpha (eIF2a) on serine 51 [19, 20] , leading to protein synthesis shut-off and apoptosis. PKR has been also been shown to participate in several important signaling cascades, including the p38 and JNK pathways [21] , as well as type-I IFN production [22, 23] . Inhibition of translation, IFN responses and triggering of apoptosis combine to make PKR a powerful antiviral molecule, and many viruses have evolved strategies to antagonize it [24, 25] . Interestingly, several positive RNA-strand viruses (eg. Togaviridae or Picornaviridae) have been shown to activate PKR, resulting in phosphorylation of eIF2a and host translation arrest [26] , while viral mRNA could initiate translation in an eIF2-independent manner by means of a dedicated RNA structure, that stalls the scanning 40S ribosome on the initiation codon [25] .