Pathogenèse de l'infection par le SARS-CoV-2
PATHOGENESIS OF SARS-COV-2 INFECTION COVID-19 follows a rather stereotyped and reproducible course. While the first events are mediated by direct viral toxicity, resolution of the infection relies on a finely tuned immune response. In patients with severe forms, defects of the initial immune response have been reported, including insufficient type 1 interferon production or signaling, attenuated or skewed adaptative immune response, sometimes due to viral immune escape properties. These defects induce an hyperinflammatory state featuring hypersecretion of pro-inflammatory cytokines, excessive recruitment of immune cells in the lungs and parenchymal lesions, responsible for COVID-19 acute respiratory distress syndrome. Thus, COVID-19 is successively a viral and an inflammatory disease. Clarifying the chronology of these viral and immunological mechanisms allows us to identify a therapeutic logic, which sometimes involves contradictory treatments.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2022 |
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Erschienen: |
2022 |
Enthalten in: |
Zur Gesamtaufnahme - volume:72 |
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Enthalten in: |
La Revue du praticien - 72(2022), 5 vom: 06. Mai, Seite 501-504 |
Sprache: |
Französisch |
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Weiterer Titel: |
Infection with SARS-CoV-2 : a viral or inflammatory disease ? |
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Beteiligte Personen: |
Richier, Quentin [VerfasserIn] |
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Themen: |
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Anmerkungen: |
Date Completed 29.07.2022 Date Revised 29.07.2022 published: Print Citation Status MEDLINE |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM344193780 |
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520 | |a PATHOGENESIS OF SARS-COV-2 INFECTION COVID-19 follows a rather stereotyped and reproducible course. While the first events are mediated by direct viral toxicity, resolution of the infection relies on a finely tuned immune response. In patients with severe forms, defects of the initial immune response have been reported, including insufficient type 1 interferon production or signaling, attenuated or skewed adaptative immune response, sometimes due to viral immune escape properties. These defects induce an hyperinflammatory state featuring hypersecretion of pro-inflammatory cytokines, excessive recruitment of immune cells in the lungs and parenchymal lesions, responsible for COVID-19 acute respiratory distress syndrome. Thus, COVID-19 is successively a viral and an inflammatory disease. Clarifying the chronology of these viral and immunological mechanisms allows us to identify a therapeutic logic, which sometimes involves contradictory treatments | ||
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