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Article: Gastrointestinal Manifestations of SARS-CoV-2: Transmission, Pathogenesis, Immunomodulation, Microflora Dysbiosis, and Clinical Implications

TitleGastrointestinal Manifestations of SARS-CoV-2: Transmission, Pathogenesis, Immunomodulation, Microflora Dysbiosis, and Clinical Implications
Authors
Keywordsangiotensin-converting enzyme 2
COVID-19
gastroenteritis
gut microflora
immune responses
inflammatory bowel disease
pathogenesis
SARS-CoV-2
therapeutics
Issue Date24-May-2023
PublisherMDPI
Citation
Viruses, 2023, v. 15, n. 6 How to Cite?
Abstract

The clinical manifestation of COVID-19, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), in the respiratory system of humans is widely recognized. There is increasing evidence suggesting that SARS-CoV-2 possesses the capability to invade the gastrointestinal (GI) system, leading to the manifestation of symptoms such as vomiting, diarrhea, abdominal pain, and GI lesions. These symptoms subsequently contribute to the development of gastroenteritis and inflammatory bowel disease (IBD). Nevertheless, the pathophysiological mechanisms linking these GI symptoms to SARS-CoV-2 infection remain unelucidated. During infection, SARS-CoV-2 binds to angiotensin-converting enzyme 2 and other host proteases in the GI tract during the infection, possibly causing GI symptoms by damaging the intestinal barrier and stimulating inflammatory factor production, respectively. The symptoms of COVID-19-induced GI infection and IBD include intestinal inflammation, mucosal hyperpermeability, bacterial overgrowth, dysbiosis, and changes in blood and fecal metabolomics. Deciphering the pathogenesis of COVID-19 and understanding its exacerbation may provide insights into disease prognosis and pave the way for the discovery of potential novel targets for disease prevention or treatment. Besides the usual transmission routes, SARS-CoV-2 can also be transmitted via the feces of an infected person. Hence, it is crucial to implement preventive and control measures in order to mitigate the fecal-to-oral transmission of SARS-CoV-2. Within this context, the identification and diagnosis of GI tract symptoms during these infections assume significance as they facilitate early detection of the disease and the development of targeted therapeutics. The present review discusses the receptors, pathogenesis, and transmission of SARS-CoV-2, with a particular focus on the induction of gut immune responses, the influence of gut microbes, and potential therapeutic targets against COVID-19-induced GI infection and IBD.


Persistent Identifierhttp://hdl.handle.net/10722/356377
ISSN
2023 Impact Factor: 3.8
2023 SCImago Journal Rankings: 1.140
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDurairajan, Siva Sundara Kumar-
dc.contributor.authorSingh, Abhay Kumar-
dc.contributor.authorSaravanan, Udhaya Bharathy-
dc.contributor.authorNamachivayam, Mayurikaa-
dc.contributor.authorRadhakrishnan, Moorthi-
dc.contributor.authorHuang, Jian Dong-
dc.contributor.authorDhodapkar, Rahul-
dc.contributor.authorZhang, Hongjie-
dc.date.accessioned2025-05-30T00:35:31Z-
dc.date.available2025-05-30T00:35:31Z-
dc.date.issued2023-05-24-
dc.identifier.citationViruses, 2023, v. 15, n. 6-
dc.identifier.issn1999-4915-
dc.identifier.urihttp://hdl.handle.net/10722/356377-
dc.description.abstract<p>The clinical manifestation of COVID-19, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), in the respiratory system of humans is widely recognized. There is increasing evidence suggesting that SARS-CoV-2 possesses the capability to invade the gastrointestinal (GI) system, leading to the manifestation of symptoms such as vomiting, diarrhea, abdominal pain, and GI lesions. These symptoms subsequently contribute to the development of gastroenteritis and inflammatory bowel disease (IBD). Nevertheless, the pathophysiological mechanisms linking these GI symptoms to SARS-CoV-2 infection remain unelucidated. During infection, SARS-CoV-2 binds to angiotensin-converting enzyme 2 and other host proteases in the GI tract during the infection, possibly causing GI symptoms by damaging the intestinal barrier and stimulating inflammatory factor production, respectively. The symptoms of COVID-19-induced GI infection and IBD include intestinal inflammation, mucosal hyperpermeability, bacterial overgrowth, dysbiosis, and changes in blood and fecal metabolomics. Deciphering the pathogenesis of COVID-19 and understanding its exacerbation may provide insights into disease prognosis and pave the way for the discovery of potential novel targets for disease prevention or treatment. Besides the usual transmission routes, SARS-CoV-2 can also be transmitted via the feces of an infected person. Hence, it is crucial to implement preventive and control measures in order to mitigate the fecal-to-oral transmission of SARS-CoV-2. Within this context, the identification and diagnosis of GI tract symptoms during these infections assume significance as they facilitate early detection of the disease and the development of targeted therapeutics. The present review discusses the receptors, pathogenesis, and transmission of SARS-CoV-2, with a particular focus on the induction of gut immune responses, the influence of gut microbes, and potential therapeutic targets against COVID-19-induced GI infection and IBD.</p>-
dc.languageeng-
dc.publisherMDPI-
dc.relation.ispartofViruses-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectangiotensin-converting enzyme 2-
dc.subjectCOVID-19-
dc.subjectgastroenteritis-
dc.subjectgut microflora-
dc.subjectimmune responses-
dc.subjectinflammatory bowel disease-
dc.subjectpathogenesis-
dc.subjectSARS-CoV-2-
dc.subjecttherapeutics-
dc.titleGastrointestinal Manifestations of SARS-CoV-2: Transmission, Pathogenesis, Immunomodulation, Microflora Dysbiosis, and Clinical Implications-
dc.typeArticle-
dc.identifier.doi10.3390/v15061231-
dc.identifier.scopuseid_2-s2.0-85164017848-
dc.identifier.volume15-
dc.identifier.issue6-
dc.identifier.eissn1999-4915-
dc.identifier.isiWOS:001015864500001-
dc.identifier.issnl1999-4915-

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