EIF2AK2 and infection: K3L acts as a pseudo-substrate of PKR to competitively inhibit PKR from binding eIF2α (Figure 2—figure supplement 1; Beattie et al., 1991; Kawagishi-Kobayashi et al., 1997), and can be essential for productive infections depending on the host (Langland and Jacobs, 2002; Park et al., 2019; Park et al., 2021).