| Summary: | 碩士 === 長庚大學 === 醫學生物技術研究所 === 94 === Accumulating evidence suggests that cellular redox status plays an important role in regulating viral replication and infectivity. Glucose 6-phosphate dehydrogenase (G6PD) deficient fibroblast has been shown to suffer higher oxidative stress than normal control part. Experiments were performed to compare the susceptibility of normal (HFF3) and G6PD-deficient (HFF1) cells to enterovirus71 (EV71) infection. After EV71 infection, both types of cells developed cytopathic effect. G6PD deficiency cells to predispose cell death in response to EV71 infection : cell viability of HFF1 was 32.4 ± 10.0 % of uninfected control whereas the viability of HFF3 was 50.6 ± 10.4 % of uninfected control .The level of progeny virus from HFF1 (2.16 ± 0.31 × 105) was 2 fold higher than that of HFF3 (9.0 ± 2.8 × 104) at 1.25 M.O.I. 48h post-infection. This data consistent with the increased expression of viral protein and increased copy number of viral genomic RNA in HFF1. In addition, ectopic expression of G6PD in the deficient cells increased their viability upon viral infection, this was associated with reduced viral replication. Furthermore, virus infection caused gradient reduction in the ratio of the level of GSH/GSSG in both type of cells. Moreover, pre-treatment antioxidant, such as Epigallocatechin gallate (EGCG) or Pistacia weinmannifolia (PW), was able to increase cell viability and inhibit viral replication in both types of cells following EV71 infection. Taken together, these data support our hypothesis that G6PD-deficient cells are highly susceptible to EV71 infection and EGCG pre-treatment can reduce the toxicity upon EV71 infection.
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