Taken together, the results from trans-ISRIB and AMG PERK 44 treatment suggest that both FB and MVE undergo stress response activation during infection, which is exacerbated when the ability to slow translation through eIF2alpha phosphorylation is removed, and that viral production is dependent on non-eIF2alpha-related signaling through PERK kinase. The gene discussed is EIF2S1; the disease is infection.