2020
DOI: 10.1053/j.gastro.2020.04.006
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Why Does SARS-CoV-2 Invade the Gastrointestinal Epithelium?

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Cited by 29 publications
(29 citation statements)
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“…There is a furan cleavage site at the boundary between S1 and S2 subunits, which is mutated during virus invasion, thus distinguishing SARS-CoV-2 from SARS-CoV [16]. Veesler et al showed that SARS-CoV-2 entered cells using S protein by utilizing the angiotensin-converting enzyme 2 (ACE2) receptor on the surface of host cells, which is widely present in human respiratory and intestinal mucosal epithelial cells, enabling SARS-CoV-2 to infect humans and cause transmission in humans, which is similar to the transmission mechanism of SARS-CoV [16,19]. In addition, studies have shown that the expression level of ACE2 gene in the lungs of smokers is significantly higher than that of non-smokers, and smokers are more likely to be infected with SARS-CoV-2 [20].…”
Section: Virologymentioning
confidence: 99%
“…There is a furan cleavage site at the boundary between S1 and S2 subunits, which is mutated during virus invasion, thus distinguishing SARS-CoV-2 from SARS-CoV [16]. Veesler et al showed that SARS-CoV-2 entered cells using S protein by utilizing the angiotensin-converting enzyme 2 (ACE2) receptor on the surface of host cells, which is widely present in human respiratory and intestinal mucosal epithelial cells, enabling SARS-CoV-2 to infect humans and cause transmission in humans, which is similar to the transmission mechanism of SARS-CoV [16,19]. In addition, studies have shown that the expression level of ACE2 gene in the lungs of smokers is significantly higher than that of non-smokers, and smokers are more likely to be infected with SARS-CoV-2 [20].…”
Section: Virologymentioning
confidence: 99%
“…Although gastric acid can significantly reduce virus viability, SARS-CoV-2 is not inactivated in the stomach at gastric pH higher than 3.0 at room temperature [ 39 , 40 ]. This suggests the possibility that the virus travels to the intestine by passing through the gastric acid barrier, at least under conditions of chronic gastritis or Helicobacter pylori infection, the use of gastric acid inhibitors, or previous gastrectomy [ 41 ]. However, to date, several studies exploring the association between the use of proton pump inhibitors and increased disease severity/susceptibility to COVID-19 are controversial [ 42 , 43 , 44 ], making it difficult to determine whether there is indeed an increased risk for SARS-CoV-2 infection and COVID-19-related death for users of proton pump inhibitors.…”
Section: Clinical Gi Featuresmentioning
confidence: 99%
“…Since SARS-CoV is completely inactivated by gastric pH ( 20 ), it is plausible that the replication of SARS-CoV-2 in the GIT may have become resistent to an increase in the gastric pH due to atrophic gastritis, gastric intestinal metaplasia, Helicobacter pylori infection, or the prolonged use of proton pump inhibitors ( 5 , 21 ). The presence of the coronavirus in the feces cannot be justified only by the swallowing saliva containing the virus because fecal swabs often remain positive even when pharyngeal swabs are negative ( 21 , 22 ).…”
Section: Discussionmentioning
confidence: 99%