The type I interferon response during viral infections: a “SWOT” analysis
Identifieur interne : 000B98 ( Main/Exploration ); précédent : 000B97; suivant : 000B99The type I interferon response during viral infections: a “SWOT” analysis
Auteurs : Giel R. Gaajetaan [Pays-Bas] ; Cathrien A. Bruggeman [Pays-Bas] ; Frank R. Stassen [Pays-Bas]Source :
- Reviews in Medical Virology [ 1052-9276 ] ; 2012-03.
English descriptors
- Teeft :
- Adaptive, Agonist, Antiviral, Antiviral drugs, Antiviral effects, Antiviral proteins, Antiviral research, Antiviral response, Autoimmune diseases, Cell surface, Chronic hepatitis, Clinical application, Copyright, Cytoid dendritic cells, Cytokine, Cytoplasmic, Cytoplasmic prrs, Dendritic, Dendritic cells, Dsrna, Epithelial cells, Experimental medicine, Gaajetaan, Herpes, Ifna, Ifnar, Ifnb, Ifns, Immu, Immune, Immune cells, Immune response, Immune system, Immune therapy, Immunology, Infection, Infectious diseases, Innate, Innate immunity, Interferon, Interferon receptor, Interferon response, Interferon response factor, Intracellular, Irf3, Irf7, Isgs, John wiley sons, Lectin receptors, Ligand, Mda5, National academy, Nature immunology, Nature reviews immunology, Nucleic, Nucleic acids, Other hand, Pathway, Pattern recognition receptors, Pdcs, Peripheral blood, Plasmacytoid, Plasmacytoid dendritic cells, Prrs, Receptor, Receptor ligands, Replication, Restriction factors, Sars, Side effects, Systemic lupus erythematosus, Tlr7, Tlr8, Tlr9, Tlrs, Vaccine, Viral, Viral disease, Viral infection, Viral infections, Viral recognition, Viral replication, Virol, Virology, Virus, Wang.
Abstract
The type I interferon (IFN) response is a strong and crucial moderator for the control of viral infections. The strength of this system is illustrated by the fact that, despite some temporary discomfort like a common cold or diarrhea, most viral infections will not cause major harm to the healthy immunocompetent host. To achieve this, the immune system is equipped with a wide array of pattern recognition receptors and the subsequent coordinated type I IFN response orchestrated by plasmacytoid dendritic cells (pDCs) and conventional dendritic cells (cDCs). The production of type I IFN subtypes by dendritic cells (DCs), but also other cells is crucial for the execution of many antiviral processes. Despite this coordinated response, morbidity and mortality are still common in viral disease due to the ability of viruses to exploit the weaknesses of the immune system. Viruses successfully evade immunity and infection can result in aberrant immune responses. However, these weaknesses also open opportunities for improvement via clinical interventions as can be seen in current vaccination and antiviral treatment programs. The application of IFNs, Toll‐like receptor ligands, DCs, and antiviral proteins is now being investigated to further limit viral infections. Unfortunately, a common threat during stimulation of immunity is the possible initiation or aggravation of autoimmunity. Also the translation from animal models to the human situation remains difficult. With a Strengths–Weaknesses–Opportunities–Threats (“SWOT”) analysis, we discuss the interaction between host and virus as well as (future) therapeutic options, related to the type I IFN system. Copyright © 2011 John Wiley & Sons, Ltd.
Url:
DOI: 10.1002/rmv.713
Affiliations:
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The strength of this system is illustrated by the fact that, despite some temporary discomfort like a common cold or diarrhea, most viral infections will not cause major harm to the healthy immunocompetent host. To achieve this, the immune system is equipped with a wide array of pattern recognition receptors and the subsequent coordinated type I IFN response orchestrated by plasmacytoid dendritic cells (pDCs) and conventional dendritic cells (cDCs). The production of type I IFN subtypes by dendritic cells (DCs), but also other cells is crucial for the execution of many antiviral processes. Despite this coordinated response, morbidity and mortality are still common in viral disease due to the ability of viruses to exploit the weaknesses of the immune system. Viruses successfully evade immunity and infection can result in aberrant immune responses. However, these weaknesses also open opportunities for improvement via clinical interventions as can be seen in current vaccination and antiviral treatment programs. The application of IFNs, Toll‐like receptor ligands, DCs, and antiviral proteins is now being investigated to further limit viral infections. Unfortunately, a common threat during stimulation of immunity is the possible initiation or aggravation of autoimmunity. Also the translation from animal models to the human situation remains difficult. With a Strengths–Weaknesses–Opportunities–Threats (“SWOT”) analysis, we discuss the interaction between host and virus as well as (future) therapeutic options, related to the type I IFN system. Copyright © 2011 John Wiley & Sons, Ltd.</div></front></TEI><affiliations><list><country><li>Pays-Bas</li></country></list><tree><country name="Pays-Bas"><noRegion><name sortKey="Gaajetaan, Giel R" sort="Gaajetaan, Giel R" uniqKey="Gaajetaan G" first="Giel R." last="Gaajetaan">Giel R. 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