Abstract
Infection with SARS-CoV-2 causes the coronavirus infectious disease 2019 (COVID-19), a pandemic that has, at present, infected more than 11 million people globally. Some COVID-19 patients develop a severe and critical illness, spurred on by excessive inflammation that can lead to respiratory or multiorgan failure. Numerous studies have established the unique array of cytoprotective properties of the dietary amino acid ergothioneine. Based on studies in a range of in vitro and in vivo models, ergothioneine has exhibited the ability to modulate inflammation, scavenge free radicals, protect against acute respiratory distress syndrome, prevent endothelial dysfunction, protect against ischemia and reperfusion injury, protect against neuronal damage, counteract iron dysregulation, hinder lung and liver fibrosis, and mitigate damage to the lungs, kidneys, liver, gastrointestinal tract, and testis, amongst many others. When compiled, this evidence suggests that ergothioneine has a potential application in the treatment of the underlying pathology of COVID-19. We propose that ergothioneine could be used as a therapeutic to reduce the severity and mortality of COVID-19, especially in the elderly and those with underlying health conditions. This review presents evidence to support that proposal.
Highlights
Coronaviruses and COVID-19Coronaviruses consisting of an enveloped, nonsegmented positive-sense RNA are the largest group of viruses [1]
Ergothioneine (ET; refer to [24,25,26] for detailed overviews of ET) is a naturally occurring dietary amino acid that is able to accumulate in most cells and tissues in the body due to the presence of the organic cation transporter novel-type 1 (OCTN1), which has a specific role in ET transport as first uncovered by Grundemann et al [24,26,27,28]
There may be multiple mechanisms by which COVID-19 can lead to neurological symptoms, including respiratory distress leading to hypoxia, cytokine storm-induced inflammatory damage to the central nervous system (CNS), the hypercoagulable state leading to cerebral venous thrombosis or stroke, or by direct SARS-CoV-2 invasion of the brain
Summary
Coronaviruses consisting of an enveloped, nonsegmented positive-sense RNA are the largest group of viruses [1] They cause a range of respiratory and intestinal infections in animals and humans but were not considered to be highly pathogenic in humans until two novel variants, the severe acute respiratory syndrome coronavirus (SARS-CoV) in 2002 [2], and a decade later, the Middle East respiratory syndrome (MERS) CoV [3], brought global awareness to their infectivity and lethality. The infection of the human respiratory epithelium by SARS CoV-2 results in the coronavirus infectious disease 2019 (COVID-19). The most common clinical symptoms for COVID-19 are similar to earlier coronavirus infections (i.e., the SARS CoV and MERS CoV), with fever present in close to 90% of cases and more than two-thirds developing cough [15]. Much remains unknown about the actual underlying pathophysiology of the disease, and more data are urgently needed to further understand the processes leading to morbidity and mortality in COVID-19
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