G6PD-deficiency enhances the infectivity of enterovius 71 human foreskin fibroblast
碩士 === 長庚大學 === 醫學生物技術研究所 === 92 === Accumulating evidence suggests that cellular redox status plays an important role in regulating viral replication and infectivity. G6PD-deficient human foreskin fibroblast (HFF) is under increased oxidative stress. In this study, experiments were performed to com...
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ndltd-TW-092CGU006040082016-01-04T04:08:38Z http://ndltd.ncl.edu.tw/handle/08883868246248175846 G6PD-deficiency enhances the infectivity of enterovius 71 human foreskin fibroblast 「G6PD缺乏」增強腸病毒71型對於人類纖維母細胞的感染能力 葉純純 碩士 長庚大學 醫學生物技術研究所 92 Accumulating evidence suggests that cellular redox status plays an important role in regulating viral replication and infectivity. G6PD-deficient human foreskin fibroblast (HFF) is under increased oxidative stress. In this study, 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. There was a significant difference ( p < 0.05) in cell viability of both types of cells: cell viability of HFF1 was 30% of uninfected control whereas the viability of HFF3 was 42% of uninfected control. The amount of viral particles collected from HFF1 (5.4×104 PFU/ml) was greater than that of HFF3 (2.0×104 PFU/ml). Consistent with the ectopic expression of G6PD in the deficient cells increased their viability upon viral infection, and at the same time, reduced viral replication. Moreover, the level of the viral gene (3C) expression was increased by more than 2 folds in G6PD-deficient cells as compared to G6PD-overexpression cells by quantitative PCR. The GSH/GSSG ratio in G6PD-deficient cells was lower than G6PD over-expression cells. Taken together, our new findings support the notion that G6PD-deficient cells are more susceptible to EV71 infection. 趙崇義 施信如 鄭美玲助理 何鴻耀助理 2004 學位論文 ; thesis 44 zh-TW |
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碩士 === 長庚大學 === 醫學生物技術研究所 === 92 === Accumulating evidence suggests that cellular redox status plays an important role in regulating viral replication and infectivity. G6PD-deficient human foreskin fibroblast (HFF) is under increased oxidative stress. In this study, 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. There was a significant difference ( p < 0.05) in cell viability of both types of cells: cell viability of HFF1 was 30% of uninfected control whereas the viability of HFF3 was 42% of uninfected control. The amount of viral particles collected from HFF1 (5.4×104 PFU/ml) was greater than that of HFF3 (2.0×104 PFU/ml). Consistent with the ectopic expression of G6PD in the deficient cells increased their viability upon viral infection, and at the same time, reduced viral replication. Moreover, the level of the viral gene (3C) expression was increased by more than 2 folds in G6PD-deficient cells as compared to G6PD-overexpression cells by quantitative PCR. The GSH/GSSG ratio in G6PD-deficient cells was lower than G6PD over-expression cells. Taken together, our new findings support the notion that G6PD-deficient cells are more susceptible to EV71 infection.
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趙崇義 |
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趙崇義 葉純純 |
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葉純純 |
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葉純純 G6PD-deficiency enhances the infectivity of enterovius 71 human foreskin fibroblast |
author_sort |
葉純純 |
title |
G6PD-deficiency enhances the infectivity of enterovius 71 human foreskin fibroblast |
title_short |
G6PD-deficiency enhances the infectivity of enterovius 71 human foreskin fibroblast |
title_full |
G6PD-deficiency enhances the infectivity of enterovius 71 human foreskin fibroblast |
title_fullStr |
G6PD-deficiency enhances the infectivity of enterovius 71 human foreskin fibroblast |
title_full_unstemmed |
G6PD-deficiency enhances the infectivity of enterovius 71 human foreskin fibroblast |
title_sort |
g6pd-deficiency enhances the infectivity of enterovius 71 human foreskin fibroblast |
publishDate |
2004 |
url |
http://ndltd.ncl.edu.tw/handle/08883868246248175846 |
work_keys_str_mv |
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