In the adverse effects of ER stress, the p-PERK and p-eIF2α, two crucial proteins in UPR pathway (55), were activated to minimize ER dysfunction in SVV-infected cells compared to that in Mock-infected cells, while the cleaved-caspase 3 was enhanced by the continuous infection of SVV, suggesting a possible relationship between ER stress and apoptosis in SVV-infected cells. The gene discussed is CASP3; the disease is infection.