Since neither virus infection nor CoV2 or OC43 Nsp1 overexpression affect total eIF2α levels in our experiments, suppression of eIF2α phosphorylation by Nsp1 could be through direct inhibition of a specific kinase (e.g. HRI) or through stimulation of eIF2α dephosphorylation. The gene discussed is EIF2A; the disease is viral infectious disease.