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Clinical and Virus Surveillance After the First Wheezing Episode: Special Reference to Rhinovirus A and C Species

Turunen, Riitta MD*†; Vuorinen, Tytti MD†‡; Bochkov, Yury PhD§; Gern, James MD§; Jartti, Tuomas MD*

The Pediatric Infectious Disease Journal: June 2017 - Volume 36 - Issue 6 - p 539–544
doi: 10.1097/INF.0000000000001495
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Background: Susceptibility to rhinovirus (RV)-induced early wheezing episode has been recognized as an important risk factor for asthma, but the data on different RV species are limited. Our aim was to investigate the risk for recurrences in first-time wheezing children with special focus on RV species.

Methods: First-time wheezing children (88 inpatients and 23 outpatients) were prospectively followed at 2-week, 2-month and 12-month time-points, and at first recurrence within 12 months. The respiratory virus etiology was analyzed using polymerase chain reaction. RV-positive samples were sequenced. The primary outcomes were time to a new physician-confirmed wheezing episode, time to a new RV-induced wheezing episode and time to the initiation of regular controller medication for asthma symptoms.

Results: The median age of the children was 12 months (standard deviation, 6.0), 67% were males and 23% were sensitized. RV dominated in symptomatic and asymptomatic infections. Different RV strains were observed in 97% (67/69) of consecutive samples during follow-up. First-time wheezing children with RV-C and RV-A had an increased risk for a new physician-confirmed wheezing episode and a new RV-associated wheezing episode than non-RV group (all P < 0.05). Also, the risk for the initiation of regular controller medication was increased in RV-A and RV-C groups when compared with non-RV group (both P < 0.05).

Conclusions: RV causes reinfections with different strains in small children after the first wheezing episode. Both RV-A and RV-C affected children have an increased risk for recurrence, especially RV associated, and initiation of regular controller medication than those with other viruses.

Supplemental Digital Content is available in the text.

From the *Department of Pediatrics, University of Turku and Turku University Hospital, Turku, Finland; Department of Virology, University of Turku, Turku, Finland; Department of Clinical Virology, Division of Microbiology and Genetics, Turku University Hospital, Turku, Finland; and §The Departments of Pediatrics and Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.

Accepted for publication October 6, 2016.

Supported by grants from the Foundation for Pediatric Research (Helsinki), Allergy Research Foundation in Southwest Finland (Turku), the Sigrid Juselius Foundation (Helsinki), the Academy of Finland (Grant nos. 132595 and 114034) (Helsinki), the Finnish Medical Foundation (Helsinki), Turku University Foundation (Turku), The TYKS Foundation (Turku), Tampere Tuberculosis Foundation (Tampere), Ida Montin Foundation (Espoo), the Research Foundation of the Pulmonary Diseases (Helsinki) and The Finnish Cultural Foundation (Helsinki) (all in Finland).

The authors have no conflicts of interest to disclose.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www.pidj.com).

Address for correspondence: Riitta Turunen, MD, Vinku Study Group, Department of Pediatrics, Turku University Hospital, P.O. Box 52, FIN-20520 Turku, Finland. E-mail: riitta.turunen@utu.fi.

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