Type I and III IFN-mediated antiviral actions counteracted by SARS-CoV-2 proteins and host inherited factors

Autor:	Jorge Quarleri, M. Victoria Delpino
Rok vydání:	2021
Předmět:	0301 basic medicine viruses Endocrinology Diabetes and Metabolism IFNAR type I IFN receptor IKKε IκB kinase-ε Disease LGP2 laboratory of genetics and physiology-2 IRF IFN regulatory factor medicine.disease_cause IκB inhibitor of nuclear factor κB TLRs Toll-like receptors Interferon Lambda IFITM interferon-induced transmembrane proteins AAV adeno-associated virus 0302 clinical medicine PRRs pattern recognition receptors Interferon Immunology and Allergy IGFBP3 insulin-like growth factor-binding protein 3 TRAF3 tumor necrosis factor receptor-associated factor 3 SOCS suppressor of cytokine signaling proteins MOI multiplicity of infection human coronavirus Coronavirus TBK1 TANK binding kinase 1 Effector KPNA2 karyopherin-α2 HCoV human coronaviruses MERS-CoV Middle East respiratory syndrome coronavirus interferon STATs signal transducer and activator of transcription dsRNA double stranded RNA 030220 oncology & carcinogenesis Host-Pathogen Interactions Interferon Type I MAVS mitochondrial antiviral signaling protein inborn errors medicine.drug MDA5 melanoma differentiation-associated gene 5 S spike JAK1 Janus kinase 1 Tyk2 Jak tyrosine kinases tyrosine kinase 2 Immunology NPC nuclear pore complex E envelope ISGs interferon-stimulated genes ORFs open reading frames Biology ACE2 angiotensin-converting enzyme 2 Antiviral Agents SARS-CoV-2 severe acute respiratory syndrome coronavirus 2 Article General Biochemistry Genetics and Molecular Biology Virus scRNA-seq single-cell RNA-sequencing Viral Proteins 03 medical and health sciences Immune system PAMPs pathogen-associated molecular patterns M membrane medicine Animals Humans Genetic Predisposition to Disease IFN interferon SARS severe acute respiratory syndrome Pandemics KLF-5 Krüpple-like factor 5 immune evasion NF-κB transcription factors nuclear factor-κB Innate immune system SARS-CoV-2 Genetic Diseases Inborn Autoantibody COVID-19 ISRE IFN-stimulated response element HIF1α hypoxia-inducible factor-1α Immunity Innate ISGF3 IFN-stimulated growth factor 3 RIG-I retinoic acid-inducible gene 1 030104 developmental biology TBK1 TANK-binding kinase 1 TMPRSS2 transmembrane serine protease 2 Interferons TANK TRAF family member-associated NF-κB activator IFNLR IFN-λ receptor N nucleocapsid
Zdroj:	Cytokine & Growth Factor Reviews
ISSN:	1359-6101
DOI:	10.1016/j.cytogfr.2021.01.003
Popis:	SARS-CoV-2 is a recently identified coronavirus accountable for the current pandemic disease known as COVID-19. Different patterns of disease progression infer a diverse host immune response, with interferon (IFN) being pivotal. IFN-I and III are produced and released by virus-infected cells during the interplay with SARS-CoV-2, thus establishing an antiviral state in target cells. However, the efficacy of IFN and its role in the possible outcomes of the disease are not yet defined, as it is influenced both by factors inherent to the virus and to the host. The virus exhibits multiple strategies to counteract the innate immune response, including those shared by SARS-CoV and MERS-CoV and other novel ones. Inborn errors in the host may affect IFN-related effector proteins or decrease its levels in plasma upon neutralization by preexistent autoantibodies. This battle between the IFN response triggered upon SARS-CoV-2 infection, its magnitude and timing, and the efficacy of its antiviral tools in dispute against the viral evasion strategies together with the genetic factors of the host, generate a scenario whose fate contributes to defining the severity of COVID-19.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9f0ed2f72291aa86d6f23c42f116bc46 https://doi.org/10.1016/j.cytogfr.2021.01.003 Zobrazit plný text záznamu Full Text from ScienceDirect