Academic Journal
Interfering with Interferons: A Critical Mechanism for Critical COVID-19 Pneumonia
| العنوان: | Interfering with Interferons: A Critical Mechanism for Critical COVID-19 Pneumonia |
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| المؤلفون: | Su, Helen, C, Jing, Huie, Zhang, Yu, Casanova, Jean-Laurent |
| المساهمون: | National Institute of Allergy and Infectious Diseases Bethesda (NIAID-NIH), National Institutes of Health Bethesda, MD, USA (NIH), Human genetics of infectious diseases : Mendelian predisposition (Equipe Inserm U1163), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Howard Hughes Medical Institute (HHMI), St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller University New York, Hôpital Necker - Enfants Malades AP-HP, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), ANR-20-CO11-0001,AABIFNCOV,Bases génétiques et immunologiques des auto-anticorps contre les interférons de type I prédisposant aux formes sévères de COVID-19.(2020), ANR-20-CE93-0003,GENVIR,Analyse multi-omique de l'immunité anti-virale: de l'identification des circuits biologiques pertinents à la découverte de défauts monogéniques héréditaires de l'immunité chez les patients avec infections virales sévères(2020) |
| المصدر: | ISSN: 0732-0582. |
| بيانات النشر: | CCSD Annual Reviews |
| سنة النشر: | 2023 |
| مصطلحات موضوعية: | COVID-19, SARS-CoV-2, type I interferon, human genetics, anticytokine autoantibodies, [SDV]Life Sciences [q-bio] |
| الوصف: | International audience ; Infection with SARS-CoV-2 results in clinical outcomes ranging from silent or benign infection in most individuals to critical pneumonia and death in a few. Genetic studies in patients have established that critical cases can result from inborn errors of TLR3- or TLR7-dependent type I interferon immunity, or from preexisting autoantibodies neutralizing primarily IFN-α and/or IFN-ω. These findings are consistent with virological studies showing that multiple SARS-CoV-2 proteins interfere with pathways of induction of, or response to, type I interferons. They are also congruent with cellular studies and mouse models that found that type I interferons can limit SARS-CoV-2 replication in vitro and in vivo, while their absence or diminution unleashes viral growth. Collectively, these findings point to insufficient type I interferon during the first days of infection as a general mechanism underlying critical COVID-19 pneumonia, with implications for treatment and directions for future research. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| Relation: | info:eu-repo/semantics/altIdentifier/pmid/37126418; PUBMED: 37126418 |
| DOI: | 10.1146/annurev-immunol-101921-050835 |
| الاتاحة: | https://hal.science/hal-04816132 https://hal.science/hal-04816132v1/document https://hal.science/hal-04816132v1/file/annurev-immunol-101921-050835.pdf https://doi.org/10.1146/annurev-immunol-101921-050835 |
| Rights: | http://creativecommons.org/licenses/by/ ; info:eu-repo/semantics/OpenAccess |
| رقم الانضمام: | edsbas.2E2854B3 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1146/annurev-immunol-101921-050835 |
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