title: Mechanisms of virus-induced asthma exacerbations: state-of-the-art. A GA2LEN and InterAirways document.
abstract: Viral infections of the respiratory tract are the most common precipitants of acute asthma exacerbations. Exacerbations are only poorly responsive to current asthma therapies and new approaches to therapy are needed. Viruses, most frequently human rhinoviruses (RV), infect the airway epithelium, generate local and systemic immune responses, as well as neural responses, inducing inflammation and airway hyperresponsiveness. Using in vitro and in vivo experimental models the role of various proinflammatory or anti-inflammatory mediators, antiviral responses and molecular pathways that lead from infection to symptoms has been partly unravelled. In particular, mechanisms of susceptibility to viral infection have been identified and the bronchial epithelium appeared to be a key player. Nevertheless, additional understanding of the integration between the diverse elements of the antiviral response, especially in the context of allergic airway inflammation, as well as the interactions between viral infections and other stimuli that affect airway inflammation and responsiveness may lead to novel strategies in treating and/or preventing asthma exacerbations. This review presents the current knowledge and highlights areas in need of further research.
authors.affiliation: Allergy Research Center, 2nd Pediatric Clinic, University of Athens, Athens, Greece.
authors.forename: N G
authors.initials: NG
authors.lastname: Papadopoulos
authors.forename: P
authors.initials: P
authors.lastname: Xepapadaki
authors.forename: P
authors.initials: P
authors.lastname: Mallia
authors.forename: G
authors.initials: G
authors.lastname: Brusselle
authors.forename: J-B
authors.initials: JB
authors.lastname: Watelet
authors.forename: M
authors.initials: M
authors.lastname: Xatzipsalti
authors.forename: G
authors.initials: G
authors.lastname: Foteinos
authors.forename: C M
authors.initials: CM
authors.lastname: van Drunen
authors.forename: W J
authors.initials: WJ
authors.lastname: Fokkens
authors.forename: C
authors.initials: C
authors.lastname: D'Ambrosio
authors.forename: S
authors.initials: S
authors.lastname: Bonini
authors.forename: A
authors.initials: A
authors.lastname: Bossios
authors.forename: Jan
authors.initials: J
authors.lastname: Lötvall
authors.forename: P
authors.initials: P
authors.lastname: van Cauwenberge
authors.forename: S T
authors.initials: ST
authors.lastname: Holgate
authors.forename: G W
authors.initials: GW
authors.lastname: Canonica
authors.forename: A
authors.initials: A
authors.lastname: Szczeklik
authors.forename: G
authors.initials: G
authors.lastname: Rohde
authors.forename: J
authors.initials: J
authors.lastname: Kimpen
authors.forename: A
authors.initials: A
authors.lastname: Pitkäranta
authors.forename: M
authors.initials: M
authors.lastname: Mäkelä
authors.forename: P
authors.initials: P
authors.lastname: Chanez
authors.forename: J
authors.initials: J
authors.lastname: Ring
authors.forename: S L
authors.initials: SL
authors.lastname: Johnston
mesh_terms: D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology / Q000821:virology*; D006801:Humans; D010850:Picornaviridae Infections / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology / Q000821:virology