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Original Research: Genetic and Developmental Disorders |

High Rhinovirus Burden in Lower Airways of Children With Cystic FibrosisHigh Rhinovirus Burden in Cystic Fibrosis

Elisabeth Kieninger, MD, PhD; Florian Singer, MD; Caroline Tapparel, PhD; Marco P. Alves, PhD; Philipp Latzin, MD, PhD; Hui-Leng Tan, MD; Cara Bossley, MD; Carmen Casaulta, MD; Andrew Bush, MD; Jane C. Davies, MD; Laurent Kaiser, MD; Nicolas Regamey, MD
Author and Funding Information

From the Division of Pediatric Respiratory Medicine (Drs Kieninger, Singer, Alves, Latzin, Casaulta, and Regamey), Department of Pediatrics, University Hospital, Bern, Switzerland; Department of Clinical Research (Drs Kieninger, Alves, Latzin, and Regamey), University of Bern, Bern, Switzerland; Laboratory of Virology (Drs Tapparel and Kaiser), Division of Infectious Diseases and Division of Laboratory Medicine, University of Geneva Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland; and the Department of Pediatric Respiratory Medicine (Drs Tan, Bossley, Bush, and Davies), Royal Brompton Hospital, London, England.

Correspondence to: Nicolas Regamey, MD, Division of Respiratory Medicine, Department of Pediatrics, University Hospital, Inselspital, 3010 Bern, Switzerland; e-mail: nicolas.regamey@insel.ch


Funding/Support: This study was supported by the Swiss National Science Foundation [Grant PP00P3_123453/1 to Dr Regamey and 32003B_127160 to Dr Kaiser], the Fondazione Ettore e Valeria Rossi (long-time fellowship to Dr Kieninger) and the Austrian, German, and Swiss Pediatric Respiratory Society (short-time fellowship to Dr Kieninger).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(3):782-790. doi:10.1378/chest.12-0954
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Background:  Rhinovirus (RV)-induced pulmonary exacerbations are common in cystic fibrosis (CF) and have been associated with impaired virus clearance by the CF airway epithelium in vitro. Here, we assess in vivo the association of RV prevalence and load with antiviral defense mechanisms, airway inflammation, and lung function parameters in children with CF compared with a control group and children with other chronic respiratory diseases.

Methods:  RV presence and load were measured by real-time reverse transcription-polymerase chain reaction in BAL samples and were related to antiviral and inflammatory mediators measured in BAL and to clinical parameters.

Results:  BAL samples were obtained from children with CF (n = 195), non-CF bronchiectasis (n = 40), or asthma (n = 29) and from a control group (n = 35) at a median (interquartile range [IQR]) age of 8.2 (4.0-11.7) years. RV was detected in 73 samples (24.4%). RV prevalence was similar among groups. RV load (median [IQR] × 103 copies/mL) was higher in children with CF (143.0 [13.1-1530.0]), especially during pulmonary exacerbations, compared with children with asthma (3.0 [1.3-25.8], P = .006) and the control group (0.5 [0.3-0.5], P < .001), but similar to patients with non-CF bronchiectasis (122.1 [2.7-4423.5], P = not significant). In children with CF, RV load was negatively associated with interferon (IFN)-β and IFN-λ, IL-1ra levels, and FEV1, and positively with levels of the cytokines CXCL8 and CXCL10.

Conclusions:  RV load in CF BAL is high, especially during exacerbated lung disease. Impaired production of antiviral mediators may lead to the high RV burden in the lower airways of children with CF. Whether high RV load is a cause or a consequence of inflammation needs further investigation in longitudinal studies.

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