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Great escape: how infectious SARS-CoV-2 avoids inactivation by gastric acidity and intestinal bile
  1. Malak A Esseili
  1. Food Science and Technology, Center for Food Safety, University of Georgia, Griffin, Georgia, USA
  1. Correspondence to Dr Malak A Esseili, Food Science and Technology, University of Georgia, Griffin, Georgia, USA; malak.esseili{at}uga.edu

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The study by Lee et al1 showed that the short-term current use of proton pump inhibitors (PPIs) for less than 1 month was associated with severe clinical outcomes for patients with COVID-19. The authors speculated that individuals taking PPIs had increased gastric pH, leading to higher SARS-CoV-2 viral loads associated with a severe course of COVID-19. Many studies suggested that a proportion of patients with COVID-19 experiencing GI symptoms such as diarrhoea, nausea and vomiting had overall more severe disease.2 However, it is not clearly understood how SARS-CoV-2 could survive the passage through the harsh gastric acidity and persist through the intestinal contents to infect the intestinal epithelia. It is known that the gastric pH varies greatly, depending on whether the individual is in a fasting or feeding state (between 1.23 and 6.7, respectively).3 Similarly, bile concentrations in the small intestine can fluctuate from as low as 2.6 mM in fasted state to over 15 mM in the fed state.4 Whether changes in gastric pH and bile allow the virus to escape gastric and intestinal inactivation to infect the intestine is not well understood. Therefore, to understand the effect of stomach acidity, digestive components and meals on the infectivity of swallowed SARS-CoV-2, the virus ~6 log 50% tissue infective dose (TCID50)/mL was incubated at 37°C for 60 min in simulated gastric fluid of different pH (1.5–6.0), pepsin (0–8 mg/mL), …

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Footnotes

  • Contributors MAE designed and conducted all the experiments, analysed the data and wrote the manuscript.

  • Funding Faculty startup provided by the University of Georgia (17ESSTART).

  • Disclaimer The views expressed in the submitted article are the author’s own and not an official position of the institution or funder.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.