Is glucose-6-phosphate dehydrogenase enzyme deficiency a factor in Coronavirus-19 (COVID-19) infections and deaths?

The coronavirus (COVID-19) pandemic has become today’s most important world public health problem. As of 30 March 2020, World Health Organization (WHO) has reported 638,146 confirmed cases and 30,039 deaths, and these numbers are increasing every day. Since no one can estimate the progression of this pandemic, social distancing, self-isolation and protection have been strongly recommended to stop the spread of the virus worldwide. COVID-19 is an enveloped and single-stranded RNA beta-coronavirus which is very similar to severe acute respiratory syndrome coronavirus (SARS-CoV)/SARS and Middle East respiratory syndrome coronavirus (MERS-CoV)/MERS. Those at particular risk have been the elderly and those with chronic diseases including diabetes, cardiovascular diseases, cancer and chronic respiratory diseases. These people appear to be at a greater risk of dying from COVID‐19. The current key problems to overcome are to find out epidemiological characteristics of COVID‐19 to prevent it from becoming epidemic- and pandemic-prone, and to understand the reasons why people succumb to this deadly virus [1].

Besides COVID-19 deaths in the elderly population and people with chronic diseases, 0.9% of deaths by COVID-19 have had no any confirmed chronic conditions [1]. One health condition that could be increasing mortality risk in the COVID-19 infected people is glucose-6 phosphate dehydrogenase (G6PD) enzyme deficiency, which is the most common enzyme deficiency worldwide affecting more than 400 million people and causes a variety of diseases [2]. Wu et al. reported that G6PD deficiency cells were infected with Human coronavirus (HCoV) 229E in a higher rate compared to normal cells. Additionally, G6PD status contributes to the status and survival of other viral diseases including HIV and hepatitis [3].

The role of G6PD deficiency on viral diseases may result from its potential role in oxidative stress metabolism. G6PD is the rate-limiting enzyme in the pentose phosphate pathway and responsible for the production of nicotinamide adenine dinucleotide phosphate (NADPH) involving the balance of reduced glutathione (GSH)/oxidized glutathione (GSSG) in both cytosol and mitochondria. Glutathione metabolism is a major component of the human anti-oxidant defense system; thus, decreased levels of G6PD result in increased levels of oxidative stress and impair redox imbalance [4,5]. Previous studies have confirmed that virus infection induces production of both reactive oxygen species (ROS) and reactive nitrogen species (RNS), both can damage proteins, DNA and cellular components of cells when antioxidant enzyme metabolism is impaired. Since G6PD deficiency results in the redox imbalance in the erythrocytes leading to hemolysis and tissue damage as a result of insufficient oxygen transportation, COVID-19 might increase the mortality risk of patients with G6PD deficiency [2–5].

In conclusion, the relationship between G6PD deficiency and COVID-19 infection is unknown. Although mortality risk is higher for older adults and individuals with chronic health conditions, G6PD enzyme deficiency should be taking into consideration in the risk assessment for COVID-19 pandemic. The effects of COVID-19 on G6PD deficiency need further study in order to clarify the underlying mechanisms.

Acknowledgments

The authors gratefully acknowledge use of the services and facilities of the Koç University Research Center for Translational Medicine (KUTTAM), funded by the Presidency of Turkey, Presidency of Strategy and Budget. The content is solely the responsibility of the authors and does not necessarily represent the official views of the Presidency of Strategy and Budget.

Disclosure statement

Authors declare that there is no conflict of interest.