G6PD deficiency, redox homeostasis, and viral infections: implications for SARS-CoV-2 (COVID-19)

Hung-Chi Yang; Tian-Hsiang Ma; Wen-Ye Tjong; Arnold Stern; Daniel Tsun-Yee Chiu

doi:10.1080/10715762.2020.1866757

G6PD deficiency, redox homeostasis, and viral infections: implications for SARS-CoV-2 (COVID-19)

Free Radic Res. 2021 Apr;55(4):364-374. doi: 10.1080/10715762.2020.1866757. Epub 2021 Jan 6.

Authors

Hung-Chi Yang¹, Tian-Hsiang Ma², Wen-Ye Tjong², Arnold Stern³, Daniel Tsun-Yee Chiu^{4

5}

Affiliations

¹ Department of Medical Laboratory Science and Biotechnology, Yuanpei University of Medical Technology, Hsinchu, Taiwan.
² Graduate Institute of Health Industry Technology, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan.
³ Grossman School of Medicine, New York University, New York, NY, USA.
⁴ Research Center for Chinese Herbal Medicine, Graduate Institute of Health Industry Technology, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan.
⁵ Department of Pediatric Hematology/Oncology, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan.

Abstract

The COVID-19 pandemic has so far affected more than 45 million people and has caused over 1 million deaths worldwide. Infection with SARS-CoV-2, the pathogenic agent, which is associated with an imbalanced redox status, causes hyperinflammation and a cytokine storm, leading to cell death. Glucose-6-phosphate dehydrogenase (G6PD) deficient individuals may experience a hemolytic crisis after being exposed to oxidants or infection. Individuals with G6PD deficiency are more susceptible to coronavirus infection than individuals with normally functioning G6PD. An altered immune response to viral infections is found in individuals with G6PD deficiency. Evidence indicates that G6PD deficiency is a predisposing factor of COVID-19.

Keywords: COVID-19; G6PD; NADPH; redox; virus.

Publication types

Review

MeSH terms

COVID-19* / complications
COVID-19* / epidemiology
COVID-19* / genetics
COVID-19* / metabolism
Disease Susceptibility
Glucosephosphate Dehydrogenase / genetics
Glucosephosphate Dehydrogenase / metabolism
Glucosephosphate Dehydrogenase Deficiency* / complications
Glucosephosphate Dehydrogenase Deficiency* / epidemiology
Glucosephosphate Dehydrogenase Deficiency* / genetics
Glucosephosphate Dehydrogenase Deficiency* / metabolism
Homeostasis / physiology
Humans
Oxidation-Reduction
Pandemics
SARS-CoV-2 / physiology*
Virus Diseases* / epidemiology
Virus Diseases* / genetics
Virus Diseases* / metabolism

Substances

Glucosephosphate Dehydrogenase

Grants and funding

This work was funded by the Ministry of Science and Technology, Taiwan, 10.13039/501100004663 (MOST108-2320-B-264-002 and MOST109-2320-B-264-001-MY2 to HCY, MOST109-2320-B-255-009 and MOST 109-2811-B-255-501 to DTYC). This work was also supported by Chang Gung Memorial Hospital, Linkou, 10.13039/ 501100005795 (CMRPF1J0072 to DTYC).