FIG. 7.

Model for PKR action. The presence of small amounts of dsRNA in cells, such as at the onset of viral infection, may provoke the binding of endogenous PKR to IKK, leading to NF-κB activation and potentiating the induction of IFN genes. For this function, PKR would not need its kinase function. Once IFN is synthesized, it provokes the induction of several genes, through JAK/STAT signaling, including the PKR gene. As the viral infection develops, there is an accumulation in the cytoplasm of dsRNA structures which activate PKR, the levels of which are now increased after IFN induction. As a kinase, PKR phosphorylates eIF2α and provokes the inhibition of protein synthesis, which can limit the propagation of the virus. eIF2α-P, phosphorylated eIF2α; IRF, IFN regulatory factor.