Virus-induced modulation of lower airway diseases: pathogenesis and pharmacologic approaches to treatment

التفاصيل البيبلوغرافية
العنوان: Virus-induced modulation of lower airway diseases: pathogenesis and pharmacologic approaches to treatment
المؤلفون: Richard Leigh, David Proud
المصدر: Pharmacology & Therapeutics
سنة النشر: 2014
مصطلحات موضوعية: Rhinovirus, Syk, spleen tyrosine kinase, Respiratory Tract Diseases, RIP-1, receptor interacting protein-1, Epithelial cells, ICAM-1, intercellular adhesion molecule-1, Cystic fibrosis, Human rhinovirus, OAS, 2′5′-oligoadenylate synthetase, TRAF-3, TNF receptor-associated factor-3, Pathogenesis, CCL, chemokine (C-C motif) ligand, Pharmacology (medical), Respiratory system, mda-5, melanoma differentiation-associated gene-5, Innate immunity, COPD, NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells, Airway remodeling, CXCR, C-X-C chemokine receptor, VEGF, vascular endothelial growth factor, medicine.anatomical_structure, iNOS, inducible nitric oxide synthase, PAMP, pathogen-associated molecular pattern, TRIF, TIR-domain-containing adapter-inducing interferon-β, IPS-1, interferon-β promoter stimulating protein-1, COAST, Childhood Origins of Asthma, RT-PCR, reverse transcription-polymerase chain reaction, T helper 2, Th2, GM-CSF, granulocyte–macrophage colony-stimulating factor, HRV, human rhinovirus, ERK, extracellular-signal-regulated kinase, Antiviral Agents, Virus, Article, LABA, Long-acting β2-adrenergic agonist, medicine, Animals, Humans, ISG, interferon-stimulated gene, IFN, interferon, TLR, toll-like receptor, OCT, octamer transcription factor, Asthma, Respiratory Sounds, Pharmacology, CF, cystic fibrosis, CXCL, chemokine (C-X-C motif) ligand, FADD, fas-associated protein with death domain, MUC5AC, Mucin 5AC, NO, nitric oxide, Picornaviridae Infections, business.industry, MMP-9, matrix metalloproteinase-9, medicine.disease, G-CSF, granulocyte colony-stimulating factor, ICS, inhaled corticosteroids, Immunity, Innate, respiratory tract diseases, IL, interleukin, RIG-I, retinoic acid inducible gene-I, COPD, chronic obstructive pulmonary disease, PI-3 kinase, phosphatidylinositol-4,5-bisphosphate 3-kinase, PRR, pattern recognition receptors, Immunology, RNA, ribonucleic acid, dsRNA, double-stranded RNA, RSV, respiratory syncytial virus, business, Airway, Respiratory tract, IRF, interferon regulatory factor
الوصف: Uncomplicated upper respiratory viral infections are the most common cause of days lost from work and school and exert a major economic burden. In susceptible individuals, however, common respiratory viruses, particularly human rhinoviruses, also can have a major impact on diseases that involve the lower airways, including asthma, chronic obstructive pulmonary diseases (COPD) and cystic fibrosis (CF). Respiratory virus-induced wheezing illnesses in early life are a significant risk factor for the subsequent development of asthma, and virus infections may also play a role in the development and progression of airway remodeling in asthma. It is clear that upper respiratory tract virus infections can spread to the lower airway and trigger acute attacks of asthma, COPD or CF. These exacerbations can be life-threatening, and exert an enormous burden on health care systems. In recent years we have gained new insights into the mechanisms by which respiratory viruses may induce acute exacerbations of lower airway diseases, as well as into host defense pathways that may regulate the outcomes to viral infections. In the current article we review the role of viruses in lower airway diseases, including our current understanding on pathways by which they may cause remodeling and trigger acute exacerbations. We also review the efficacy of current and emerging therapies used to treat these lower airway diseases on the outcomes due to viral infection, and discuss alternative therapeutic approaches for the management of virus-induced airway inflammation.
تدمد: 1879-016X
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9ceb543ec1943de9596fcd25ba010883
https://pubmed.ncbi.nlm.nih.gov/25550230
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....9ceb543ec1943de9596fcd25ba010883
قاعدة البيانات: OpenAIRE