G6PD may play an important role in viral infection [9–11,85]. Lack of G6PD promotes cytopathic effects and viral replication. G6PD-deficient cells are susceptible to viral infection, such as coronavirus, dengue virus, and enterovirus [9,85,86]. During human coronavirus 229E or enterovirus 71 infections in G6PD-deficient human lung fibroblasts and epithelial cells, HSCARG, a NADPH sensor, and a negative NF-κB regulator is up-regulated. Knockdown of HSCARG activates NF-κB and induces downstream antiviral gene expression, including TNF-α and MX1 [10]. Downregulation of HSCARG decreases viral gene expression, while the upregulation of HSCARG increases viral replication. This indicates that G6PD activity determines the anti-viral response mediated by HSCARG and the NF-κB pathway.