G6PD Insufficiency, Redox Equilibrium, and Viral Infections: Insinuations for SARS-CoV-2
The COVID-19 epidemic has inflicted damage on more than 4 crore 50 lakh people worldwide, resulting in over 10 lakh deaths. Infestation with the pathogenic SARS-CoV-2 virus leads to excessive inflammation and a cytokine storm, which leads to cell rupture due to a redox imbalance. The severe type of pneumonia caused by the human coronavirus (hCoV)-SARS-CoV-2 has caused heavy casualties, especially among the old age and those with comorbid illnesses all-inclusive of their age. The high mortality in African-American males, in general, raises the concern for a possible X-linked modulated process that could affect the viral pathogenesis and the immune system. When exposed to oxidants or infection, patients who lack the enzyme Glucose-6-Phosphate Dehydrogenase (G6PD) may have a haemolysis phenomenon. People with a G6PD deficiency are more prone to take up a virus than people with normal G6PD. G6PD deficiency causes a distinct immunological reaction to viral infections in people. G6PD insufficiency appears to be a predisposing factor for COVID-19 infection. Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD) is known to suppress the antioxidant system and is likely to aggravate severity of COVID-19 infection, which results in a pro-oxidant response leading to higher morbidity and mortality.