TY - JOUR
T1 - Viral infections in asthma and COPD
AU - Matsumoto, Koichiro
AU - Inoue, Hiromasa
N1 - Funding Information:
This work was supported in part by JSPS KAKENHI Grant nos. 25293192 and 24591132 , and by Health and Labour Sciences Research Grants from MHLW of Japan .
Funding Information:
Department of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University received research grants from Astellas Pharma Inc., Nippon Boehringer Ingelheim Co Ltd, and GlaxoSmithKline K K. Hiromasa Inoue received lecture fees from Nippon Boehringer Ingelheim Co Ltd, GlaxoSmithKline K K, and Kyorin Pharmaceutical Co Ltd. Koichiro Matsumoto has no potential conflict of interest.
PY - 2014/3
Y1 - 2014/3
N2 - Airway viral infections are associated with the pathogenesis of asthma and COPD. It has been argued that respiratory syncytial virus (RSV) infection in infancy is a probable causal factor in the development of pediatric asthma. RSV infections tend to induce Th2-biased immune responses in the host airways. RSV infection, atopy, and low pulmonary function in neonates may work synergistically toward the development of pediatric asthma. Human rhinovirus (HRV) is a representative virus associated with the exacerbation of asthma in both children and adults. Viral infections trigger innate immune responses including granulocytic inflammation and worsen the underlying inflammation due to asthma and COPD. The innate immune responses involve type-I and -III interferon (IFN) production, which plays an important role in anti-viral responses, and the airway epithelia of asthmatics reportedly exhibit defects in the virus-induced IFN responses, which renders these individuals more susceptible to viral infection. A similarly impaired IFN response is seen in COPD, and several investigators propose that latent adenoviral infection may be involved in COPD development. Persistent RSV infections were detected in a sub-population of patients with COPD and were associated with the accelerated decline of lung function. The virus-induced upregulation of co-inhibitory molecules in the airway epithelium partly accounts for the persistent infections. Experimental animal models for virus-asthma/COPD interactions have shed light on the underlying immune mechanisms and are expected to help develop novel approaches to treat respiratory diseases.
AB - Airway viral infections are associated with the pathogenesis of asthma and COPD. It has been argued that respiratory syncytial virus (RSV) infection in infancy is a probable causal factor in the development of pediatric asthma. RSV infections tend to induce Th2-biased immune responses in the host airways. RSV infection, atopy, and low pulmonary function in neonates may work synergistically toward the development of pediatric asthma. Human rhinovirus (HRV) is a representative virus associated with the exacerbation of asthma in both children and adults. Viral infections trigger innate immune responses including granulocytic inflammation and worsen the underlying inflammation due to asthma and COPD. The innate immune responses involve type-I and -III interferon (IFN) production, which plays an important role in anti-viral responses, and the airway epithelia of asthmatics reportedly exhibit defects in the virus-induced IFN responses, which renders these individuals more susceptible to viral infection. A similarly impaired IFN response is seen in COPD, and several investigators propose that latent adenoviral infection may be involved in COPD development. Persistent RSV infections were detected in a sub-population of patients with COPD and were associated with the accelerated decline of lung function. The virus-induced upregulation of co-inhibitory molecules in the airway epithelium partly accounts for the persistent infections. Experimental animal models for virus-asthma/COPD interactions have shed light on the underlying immune mechanisms and are expected to help develop novel approaches to treat respiratory diseases.
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U2 - 10.1016/j.resinv.2013.08.005
DO - 10.1016/j.resinv.2013.08.005
M3 - Review article
C2 - 24636264
AN - SCOPUS:84896031086
VL - 52
SP - 92
EP - 100
JO - Respiratory Investigation
JF - Respiratory Investigation
SN - 2212-5345
IS - 2
ER -