ArticlebioRxiv : the preprint server for biology2026
Systematic screen of PKR reveals genetic variants that broadly evade divergent viral pseudosubstrate inhibitors.
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Evolutionary arms races can arise at the contact surfaces between host and viral proteins, producing dynamic spaces in which genetic variants are continually pursued even while protein function must be maintained. A striking case is protein kinase R (PKR), an innate immune protein that detects viral replication and halts protein synthesis by phosphorylating the initiation factor eIF2α. PKR is targeted by many viral antagonists, including pseudosubstrate inhibitors encoded by poxviruses and ranaviruses that mimic eIF2α. We previously found that the eIF2α-binding surface of human PKR is highly malleable against the vaccinia virus pseudosubstrate inhibitor K3. Here, we screen our library of SNP-accessible PKR variants against five viral inhibitors of increasing divergence: K3 orthologs from vaccinia, variola, tanapox, and myxoma viruses, and the independently derived vIF2α from
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