Title: Interactions between Allergic Inflammation and Respiratory Viral Infections
Author: Avila, P. C.; (Date: Nov, 2000)
Journal: J Allergy Clin Immunol; V. 106; Issue: 5; Pages: 829-31
Notes: Comment
Editorial
Review
Review, Tutorial
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Title: Community Study of Role of Viral Infections in Exacerbations of Asthma in 9-11 Year Old Children
Author: Johnston, S. L.; Pattemore, P. K.; Sanderson, G.; Smith, S.; Lampe, F.; Josephs, L.; Symington, P.; O’Toole, S.; Myint, S. H.; Tyrrell, D. A.; et al.; (Date: May 13, 1995)
Journal: Bmj; V. 310; Issue: 6989; Pages: 1225-9
Abstract: OBJECTIVE–To study the association between upper and lower respiratory viral infections and acute exacerbations of asthma in schoolchildren in the community. DESIGN–Community based 13 month longitudinal study using diary card respiratory symptom and peak expiratory flow monitoring to allow early sampling for viruses. SUBJECTS–108 Children aged 9-11 years who had reported wheeze or cough, or both, in a questionnaire. SETTING–Southampton and surrounding community. MAIN OUTCOME MEASURES–Upper and lower respiratory viral infections detected by polymerase chain reaction or conventional methods, reported exacerbations of asthma, computer identified episodes of respiratory tract symptoms or peak flow reductions. RESULTS–Viruses were detected in 80% of reported episodes of reduced peak expiratory flow, 80% of reported episodes of wheeze, and in 85% of reported episodes of upper respiratory symptoms, cough, wheeze, and a fall in peak expiratory flow. The median duration of reported falls in peak expiratory flow was 14 days, and the median maximum fall in peak expiratory flow was 81 l/min. The most commonly identified virus type was rhinovirus. CONCLUSIONS–This study supports the hypothesis that upper respiratory viral infections are associated with 80-85% of asthma exacerbations in school age children.
Notes: Journal Article
Author Address: Southampton General Hospital.
Title: Persistence of Viruses in Upper Respiratory Tract of Children with Asthma
Author: Marin, J.; Jeler-Kacar, D.; Levstek, V.; Macek, V.; (Date: Jul, 2000)
Journal: J Infect; V. 41; Issue: 1; Pages: 69-72
Abstract: OBJECTIVES: Nasopharyngeal swabs of 50 asthmatic children in the symptom-free period were examined for the presence of adenoviruses, rhinoviruses and coronaviruses. A control group of 20 healthy individuals was included in this study. METHODS: A polymerase chain reaction was used to detect adenovirus DNA and rhinovirus and coronavirus complementary DNA. The fragments of amplified genetic material were visualized with the use of agarose gel electrophoresis. RESULTS: Adenovirus DNA was found in 78.4% of asthmatic children, rhinovirus RNA in 32.4% and coronavirus RNA in 2.7%. Adenovirus DNA was detected in one of the 20 nasopharyngeal swabs of healthy controls; the rest of the control samples were negative. CONCLUSIONS: The persistent presence of viruses in the upper respiratory tract of asthmatic children shows a possible connection between viral infections and asthma.
Notes: Journal Article
Author Address: Institute of Microbiology and Immunology, Medical Faculty, University of Ljubljana, Zaloaska 4, Ljubljana, 1105, Slovenia.
Title: Role of Viral Infections in Exacerbations of Asthma. Allergy Must Also Be a Factor
Author: Platts-Mills, T. A.; Rakes, G. P.; Heymann, P. W.; (Date: Sep 2, 1995)
Journal: Bmj; V. 311; Issue: 7005; Pages: 629-30
Notes: Comment
Letter
Title: Latent Adenoviral Infection Modifies the Steroid Response in Allergic Lung Inflammation
Author: Yamada, K.; Elliott, W. M.; Hayashi, S.; Brattsand, R.; Roberts, C.; Vitalis, T. Z.; Hogg, J. C.; (Date: Nov, 2000)
Journal: J Allergy Clin Immunol; V. 106; Issue: 5; Pages: 844-51
Abstract: BACKGROUND: Steroid-resistant asthma develops after adenoviral bronchiolitis. OBJECTIVE: We sought to determine the effect of steroids on allergic lung inflammation in the presence of latent adenoviral infection. METHODS: Guinea pigs with latent adenoviral (n = 12) or sham (n = 12) infections were sensitized and challenged with ovalbumin (OA) or sham sensitized and challenged with saline solution. The effect of steroids (20 mg/kg administered intraperitoneally) on OA-induced lung inflammation was examined by using quantitative histology as the outcome measure. RESULTS: Latent adenoviral infection increased CD8(+) cells in the airway wall and CD8(+) cells, macrophages, B cells, and CD4(+) cells in the lung parenchyma. Ovalbumin challenge, on the other hand, increased eosinophils, macrophages, B cells, and CD4(+) cells in both the airway wall and lung parenchyma independent of the effect of latent adenoviral infection. In the sham-infected groups steroid treatment caused the expected reduction in the eosinophilic infiltrate induced by OA challenge in the airways without affecting the other cells. In the presence of both latent adenoviral infection and OA challenge, steroid treatment had no effect on allergen-induced eosinophilia but reduced CD8(+) cells in the airways and CD8(+) cells, CD4(+) cells, and B cells in the parenchyma. CONCLUSION: Latent adenoviral infection and OA challenge result in different types of lung inflammation, and the presence of latent adenoviral infection causes OA-induced eosinophilic airway inflammation to become steroid resistant.
Notes: Journal Article
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Author Address: University of British Columbia Pulmonary Research Laboratory, St Paul’s Hospital, Vancouver, British Columbia, Canada.