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The effect of G6PD‐deficiency on coronavirus 229E infection
Author(s) -
WU YI HSUAN,
TSENG CHING PING,
CHENG MEI LIN,
HO HUNG YAO,
SHIH SHIN RU,
CHIU DANIEL TSUNYEE
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.lb71-b
Subject(s) - multiplicity of infection , infectivity , oxidative stress , coronavirus , cell culture , biology , viral replication , a549 cell , fibroblast , virus , microbiology and biotechnology , virology , chemistry , medicine , biochemistry , covid-19 , genetics , disease , pathology , infectious disease (medical specialty)
Severe Acute Respiratory Syndrome is caused by coronavirus. Accumulating evidence suggests that cellular redox status plays an important role in regulating viral replication and infectivity. To further delineate the effects of oxidative stress on the infectivity of coroanvirus, glucose‐6‐phosphate dehydrogenase (G6PD)‐deficient human fibroblasts and human lung epithelial carcinoma A549 cells treated with G6PD‐RNAi to lower G6PD activity were used as models to understand the susceptibility of host cells to human coronavirus 229E. After 24h, 48h & 72h post‐infection, cell viability of G6PD‐deficient cells determined by MTT method was significantly lower than normal cells at 0.1 multiplicity of infection. Viability of G6PD‐deficient cells was 18% (p<0.01) and 13% (p<0.01) lower than normal counterparts at 72h post‐infection in fibroblast and A549, respectively. In addition, viral particle production of G6PD‐deficient cells determined by plaque assay was much higher than that of normal controls. G6PD‐deficient cells were 6 and 12 fold higher in viral production than normal counterparts in fibroblasts and A549 cells at 24h post‐infection, respectively. Furthermore, viral replication in G6PD‐deficient cells as determined by Q‐PCR was found to be 3 fold higher than normal control after approximately 10h of incubation. Taken together, these preliminary data support our hypothesis that enhanced oxidative stress in host cells renders these cells more susceptible to human coronavirus 229E infection than control cells.