Journalartikel
Autorenliste: Herold, Susanne; Becker, Christin; Ridge, Karen M.; Budinger, G. R. Scott
Jahr der Veröffentlichung: 2015
Seiten: 1463-1478
Zeitschrift: European Respiratory Journal
Bandnummer: 45
Heftnummer: 5
ISSN: 0903-1936
eISSN: 1399-3003
Open Access Status: Bronze
DOI Link: https://doi.org/10.1183/09031936.00186214
Verlag: European Respiratory Society
Abstract:
The influenza viruses are some of the Most important human pathogens, causing substantial seasonal and pandemic morbidity and mortality. In humans, infection of the lower respiratory tract of can result in flooding of the alveolar compartment, development of acute respiratory distress syndrome and death from respiratory failure. Influenza-mediated damage of the airway, alveolar epithelium and alveolar endothelium results from a combination of: 1) intrinsic viral pathogenicity, attributable to its tropism for host airway and alveolar epithelial cells; and 2) a robust host innate immune response, which, while contributing to viral clearance, can worsen the severity of lung injury. In this review, we summarise the molecular events at the virus host interface during influenza virus infection, highlighting some of the important cellular responses. We discuss immune-mediated viral clearance, the mechanisms promoting or perpetuating lung injury, lung regeneration after influenza-induced injury, and recent advances in influenza prevention and therapy.
Zitierstile
Harvard-Zitierstil: Herold, S., Becker, C., Ridge, K. and Budinger, G. (2015) Influenza virus-induced lung injury: pathogenesis and implications for treatment, European Respiratory Journal, 45(5), pp. 1463-1478. https://doi.org/10.1183/09031936.00186214
APA-Zitierstil: Herold, S., Becker, C., Ridge, K., & Budinger, G. (2015). Influenza virus-induced lung injury: pathogenesis and implications for treatment. European Respiratory Journal. 45(5), 1463-1478. https://doi.org/10.1183/09031936.00186214
Schlagwörter
AIRWAY STEM-CELLS; ALVEOLAR EPITHELIAL-CELLS; A VIRUS; COLONY-STIMULATING FACTOR; NEURAMINIDASE INHIBITORS; N-linked glycosylation; PANDEMIC INFLUENZA; RECEPTOR-BINDING SPECIFICITY