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10.15252/embr.202051252

http://scihub22266oqcxt.onion/10.15252/embr.202051252
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33112036!7645910!33112036
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suck abstract from ncbi


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pmid33112036      EMBO+Rep 2020 ; 21 (12): e51252
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  • SARS-CoV-2 evades immune detection in alveolar macrophages #MMPMID33112036
  • Dalskov L; Mohlenberg M; Thyrsted J; Blay-Cadanet J; Poulsen ET; Folkersen BH; Skaarup SH; Olagnier D; Reinert L; Enghild JJ; Hoffmann HJ; Holm CK; Hartmann R
  • EMBO Rep 2020[Dec]; 21 (12): e51252 PMID33112036show ga
  • Respiratory infections, like the current COVID-19 pandemic, target epithelial cells in the respiratory tract. Alveolar macrophages (AMs) are tissue-resident macrophages located within the lung. They play a key role in the early phases of an immune response to respiratory viruses. AMs are likely the first immune cells to encounter SARS-CoV-2 during an infection, and their reaction to the virus will have a profound impact on the outcome of the infection. Interferons (IFNs) are antiviral cytokines and among the first cytokines produced upon viral infection. In this study, AMs from non-infectious donors are challenged with SARS-CoV-2. We demonstrate that challenged AMs are incapable of sensing SARS-CoV-2 and of producing an IFN response in contrast to other respiratory viruses, like influenza A virus and Sendai virus, which trigger a robust IFN response. The absence of IFN production in AMs upon challenge with SARS-CoV-2 could explain the initial asymptotic phase observed during COVID-19 and argues against AMs being the sources of pro-inflammatory cytokines later during infection.
  • |Antiviral Agents/immunology[MESH]
  • |COVID-19/*immunology/virology[MESH]
  • |Cells, Cultured[MESH]
  • |Cytokines/immunology[MESH]
  • |Epithelial Cells/immunology/virology[MESH]
  • |Humans[MESH]
  • |Immune Evasion[MESH]
  • |Interferon Type I/immunology[MESH]
  • |Lung/immunology/virology[MESH]
  • |Macrophages, Alveolar/*immunology/*virology[MESH]
  • |Pandemics[MESH]


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