glucose6phosphate dehydrogenase deficiency enhances enterovirus 71 infection variations in the cellular microenvironment affect the hosts susceptibility to pathogens using glucose6phosphate dehydrogenase g6pddeficient fibroblasts as a model this study demonstrated that the cellular redox status affects infectivity as well as the outcome of enterovirus 71 ev71 infection compared with their normal counterparts g6pddeficient cells supported ev71 replication more efficiently and showed greater cytopathic effect and loss of viability mechanistically viral infection led to increased oxidative stress as indicated by increased dichlorofluorescein fluorescence and a diminished ratio of glutathione gsh to its disulfide form gssg with the effect being greater in g6pddeficient cells exogenous expression of active g6pd in the deficient cells which increased the intracellular gshgssg ratio suppressed the generation of viral progeny consistent with this treatment with nacetylcysteine offered resistance to ev71 propagation and a cytoprotective effect on the infected cells these findings support the notion that g6pd status and thus redox balance is an important determinant of enteroviral infection