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10.1053/j.gastro.2020.12.001

http://scihub22266oqcxt.onion/10.1053/j.gastro.2020.12.001
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33307034!7725054!33307034
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suck abstract from ncbi


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pmid33307034      Gastroenterology 2021 ; 160 (5): 1647-1661
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  • The Gastrointestinal Tract Is an Alternative Route for SARS-CoV-2 Infection in a Nonhuman Primate Model #MMPMID33307034
  • Jiao L; Li H; Xu J; Yang M; Ma C; Li J; Zhao S; Wang H; Yang Y; Yu W; Wang J; Yang J; Long H; Gao J; Ding K; Wu D; Kuang D; Zhao Y; Liu J; Lu S; Liu H; Peng X
  • Gastroenterology 2021[Apr]; 160 (5): 1647-1661 PMID33307034show ga
  • BACKGROUND & AIMS: Gastrointestinal (GI) manifestations have been increasingly reported in patients with coronavirus disease 2019 (COVID-19). However, the roles of the GI tract in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are not fully understood. We investigated how the GI tract is involved in SARS-CoV-2 infection to elucidate the pathogenesis of COVID-19. METHODS: Our previously established nonhuman primate (NHP) model of COVID-19 was modified in this study to test our hypothesis. Rhesus monkeys were infected with an intragastric or intranasal challenge with SARS-CoV-2. Clinical signs were recorded after infection. Viral genomic RNA was quantified by quantitative reverse transcription polymerase chain reaction. Host responses to SARS-CoV-2 infection were evaluated by examining inflammatory cytokines, macrophages, histopathology, and mucin barrier integrity. RESULTS: Intranasal inoculation with SARS-CoV-2 led to infections and pathologic changes not only in respiratory tissues but also in digestive tissues. Expectedly, intragastric inoculation with SARS-CoV-2 resulted in the productive infection of digestive tissues and inflammation in both the lung and digestive tissues. Inflammatory cytokines were induced by both types of inoculation with SARS-CoV-2, consistent with the increased expression of CD68. Immunohistochemistry and Alcian blue/periodic acid-Schiff staining showed decreased Ki67, increased cleaved caspase 3, and decreased numbers of mucin-containing goblet cells, suggesting that the inflammation induced by these 2 types of inoculation with SARS-CoV-2 impaired the GI barrier and caused severe infections. CONCLUSIONS: Both intranasal and intragastric inoculation with SARS-CoV-2 caused pneumonia and GI dysfunction in our rhesus monkey model. Inflammatory cytokines are possible connections for the pathogenesis of SARS-CoV-2 between the respiratory and digestive systems.
  • |Animals[MESH]
  • |Bronchi/metabolism/pathology[MESH]
  • |COVID-19 Nucleic Acid Testing[MESH]
  • |COVID-19/immunology/metabolism/pathology/*transmission[MESH]
  • |Caspase 3/metabolism[MESH]
  • |Cytokines/immunology[MESH]
  • |Disease Models, Animal[MESH]
  • |Gastric Mucosa[MESH]
  • |Gastroenteritis/metabolism/*pathology/virology[MESH]
  • |Gastrointestinal Tract/immunology/metabolism/*pathology[MESH]
  • |Goblet Cells/pathology[MESH]
  • |Intestine, Small/metabolism/pathology[MESH]
  • |Ki-67 Antigen/metabolism[MESH]
  • |Lung/diagnostic imaging/immunology/metabolism/*pathology[MESH]
  • |Macaca mulatta[MESH]
  • |Nasal Mucosa[MESH]
  • |RNA, Viral/isolation & purification[MESH]
  • |Random Allocation[MESH]
  • |Rectum/metabolism/pathology[MESH]
  • |SARS-CoV-2[MESH]


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