G6PD deficiency: imbalance of functional dichotomy contributing to the severity of COVID-19

Author:

Mondal Abir1ORCID,Mukherjee Soumyadeep1ORCID,Dar Waseem1,Upadhyay Prince1,Ranganathan Anand2,Pati Soumya1,Singh Shailja2ORCID

Affiliation:

1. Department of Life Sciences, Neurobiology & Disease Modelling Laboratory, Host-Pathogen Interactions & Disease Modelling Group, School of Natural Sciences, Shiv Nadar University, Greater Noida, 201314, India

2. Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India

Abstract

Human COVID-19 has affected more than 491 million people worldwide. It has caused over 6.1 million deaths and has especially perpetrated a high number of casualties among the elderly and those with comorbid illnesses. COVID-19 triggers a pro-oxidant response, leading to the production of reactive oxygen species (ROS) as a common innate defense mechanism. However, ROS are regulated by a key enzyme called G6PD via the production of reduced nicotinamide adenine dinucleotide phosphate (NADPH), which controls the generation and removal of ROS in a tissue-specific manner. Therefore, a deficiency of G6PD can lead to the dysregulation of ROS, which causes a severe inflammatory response in COVID-19 patients. This report highlights the G6PD dichotomy in the regulation of ROS and inflammatory responses, as well as its deficiency in severity among COVID-19 patients.

Publisher

Future Medicine Ltd

Subject

Microbiology (medical),Microbiology

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