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10.1038/s41467-021-25030-7

http://scihub22266oqcxt.onion/10.1038/s41467-021-25030-7
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34381043!8357947!34381043
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suck abstract from ncbi


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pmid34381043      Nat+Commun 2021 ; 12 (1): 4869
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  • Temporal omics analysis in Syrian hamsters unravel cellular effector responses to moderate COVID-19 #MMPMID34381043
  • Nouailles G; Wyler E; Pennitz P; Postmus D; Vladimirova D; Kazmierski J; Pott F; Dietert K; Muelleder M; Farztdinov V; Obermayer B; Wienhold SM; Andreotti S; Hoefler T; Sawitzki B; Drosten C; Sander LE; Suttorp N; Ralser M; Beule D; Gruber AD; Goffinet C; Landthaler M; Trimpert J; Witzenrath M
  • Nat Commun 2021[Aug]; 12 (1): 4869 PMID34381043show ga
  • In COVID-19, immune responses are key in determining disease severity. However, cellular mechanisms at the onset of inflammatory lung injury in SARS-CoV-2 infection, particularly involving endothelial cells, remain ill-defined. Using Syrian hamsters as a model for moderate COVID-19, we conduct a detailed longitudinal analysis of systemic and pulmonary cellular responses, and corroborate it with datasets from COVID-19 patients. Monocyte-derived macrophages in lungs exert the earliest and strongest transcriptional response to infection, including induction of pro-inflammatory genes, while epithelial cells show weak alterations. Without evidence for productive infection, endothelial cells react, depending on cell subtypes, by strong and early expression of anti-viral, pro-inflammatory, and T cell recruiting genes. Recruitment of cytotoxic T cells as well as emergence of IgM antibodies precede viral clearance at day 5 post infection. Investigating SARS-CoV-2 infected Syrian hamsters thus identifies cell type-specific effector functions, providing detailed insights into pathomechanisms of COVID-19 and informing therapeutic strategies.
  • |*Disease Models, Animal[MESH]
  • |Alveolar Epithelial Cells/immunology[MESH]
  • |Animals[MESH]
  • |COVID-19/*immunology[MESH]
  • |Cricetinae[MESH]
  • |Cytokines/genetics/immunology[MESH]
  • |Endothelial Cells/immunology[MESH]
  • |Humans[MESH]
  • |Immunoglobulin M/immunology[MESH]
  • |Inflammation[MESH]
  • |Lung/immunology[MESH]
  • |Macrophages/immunology[MESH]
  • |Mesocricetus[MESH]
  • |Monocytes/immunology[MESH]
  • |SARS-CoV-2/immunology[MESH]
  • |Signal Transduction[MESH]
  • |T-Lymphocytes, Cytotoxic/immunology[MESH]


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