SARS-CoV-2, the pathogenic agent of COVID-19, has become the center of global attention. As of November, 2020, COVID-19 has affected more than 45 million people and caused over one million deaths worldwide [1]. The RNA virus SARS-CoV-2 is a member of the genus Betacoronavirus in the family Coronaviridae. A majority of individuals (80%) recover from the infection without hospitalisation. About 20% of patients develop serious symptoms and need oxygen therapy, while 5% of those require intensive care. The clinical manifestations of COVID-19 include fever, pneumonia, serum SARS-CoV-2 nucleic acid in the blood (RNAemia), and ground-glass opacities in the lung. Individuals with COVID-19 can exhibit cold-like symptoms; however, 15% of them have severe complications. These complications, which result in death, include sepsis, thromboembolism as well as multiple organ failure including injury of the lung, heart, liver, brain, and kidney [2–4]. Respiratory distress accompanied by a systemic inflammatory response, such as increased cytokine secretions, is common in individuals with severe COVID-19 [5–7]. In response to viral infection, dysregulated hyperinflammation leads to acute lung injury (ALI) manifest as an acute respiratory distress syndrome (ARDS). These pathological networks are closely associated with oxidative stress and an imbalanced redox status [8]. However, how glucose-6-phosphate dehydrogenase (G6PD), a well-known antioxidant enzyme as well as a pro-oxidant enzyme affects COVID-19 has not been carefully examined.