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Host and viral factors associated with severity of human rhinovirus–associated infant respiratory tract illness - 11/08/11

Doi : 10.1016/j.jaci.2010.11.041 
E. Kathryn Miller, MD, MPH a, John V. Williams, MD a, b, Tebeb Gebretsadik, MPH c, Kecia N. Carroll, MD, MPH a, William D. Dupont, PhD c, Yassir A. Mohamed, MS a, Laura-Lee Morin, MA a, Luke Heil a, Patricia A. Minton, RN d, Kimberly Woodward, BSN d, Zhouwen Liu, MS c, Tina V. Hartert, MD, MPH d,
a Department of Pediatrics, Vanderbilt University, Nashville, Tenn 
b Department of Microbiology and Immunology, Vanderbilt University, Nashville, Tenn 
c Department of Biostatistics, Vanderbilt University, Nashville, Tenn 
d Department of Medicine, Vanderbilt University, Nashville, Tenn 

Reprint requests: Tina V. Hartert, MD, MPH, Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, 6107 MCE, Nashville, TN 37232-8300.

Abstract

Background

Risk factors for severe human rhinovirus (HRV)–associated infant illness are unknown.

Objectives

We sought to examine the role of HRV infection in infant respiratory tract illness and assess viral and host risk factors for HRV-associated disease severity.

Methods

We used a prospective cohort of term, previously healthy infants enrolled during an inpatient or outpatient visit for acute upper or lower respiratory tract illness during the fall-spring months of 2004-2008. Illness severity was determined by using an ordinal bronchiolitis severity score, with higher scores indicating more severe disease. HRV was identified by means of real-time RT-PCR. The VP4/VP2 region from HRV-positive specimens was sequenced to determine species.

Results

Of 630 infants with bronchiolitis or upper respiratory tract illnesses (URIs), 162 (26%) had HRV infection; HRV infection was associated with 18% of cases of bronchiolitis and 47% of cases of URI. Among infants with HRV infection, 104 (64%) had HRV infection alone. Host factors associated with more severe HRV-associated illness included a maternal and family history of atopy (median score of 3.5 [interquartile range [IQR], 1.0-7.8] vs 2.0 [IQR, 1.0-5.2] and 3.5 [IQR, 1.0-7.5] vs 2.0 [IQR, 0-4.0]). In adjusted analyses maternal history of atopy conferred an increase in the risk for more severe HRV-associated bronchiolitis (odds ratio, 2.39; 95% CI, 1.14-4.99; P = .02). In a similar model maternal asthma was also associated with greater HRV-associated bronchiolitis severity (odds ratio, 2.49, 95% CI, 1.10-5.67; P = .03). Among patients with HRV infection, 35% had HRVA, 6% had HRVB, and 30% had HRVC.

Conclusion

HRV infection was a frequent cause of bronchiolitis and URIs among previously healthy term infants requiring hospitalization or unscheduled outpatient visits. Substantial viral genetic diversity was seen among the patients with HRV infection, and predominant groups varied by season and year. Host factors, including maternal atopy, were associated with more severe infant HRV-associated illness.

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Key words : Rhinovirus, HRVC, infants, atopy, asthma, bronchiolitis, maternal

Abbreviations used : HRV, IQR, ISAAC, OR, RSV, URI


Plan


 Supported by KL2 RR24977-03 (to E.K.M.), a Thrasher New Investigator Award (to E.K.M.), a Thrasher Research Fund Clinical Research Grant (to T.V.H.), an NIH midcareer investigator award K24 AI 077930 (to T.V.H.), UL1 RR024975 (Vanderbilt CTSA), and an NIH K01 AI070808 mentored clinical science award (to K.N.C.). T.V.H. is also supported by NIH grants U01 HL 072471, R01 AI 05884, R01 HS018454, R01 HS019669, and NIH K12 ES 015855.
 Disclosure of potential conflict of interest: E. K. Miller has received research support from Thrasher and VCTRS K12 and is a member of the American Academy of Allergy, Asthma & Immunology’s EORD Committee. J. V. Williams has served as a consultant for MedImmune and Novartis and serves on the scientific advisory board for Quidel. K. N. Carroll has received research support from the National Institute of Allergy and Infectious Diseases (NIAID)/National Institutes of Health (NIH). W. D. Dupont has received research support from the NIH. T. V. Hartert is on the Scientific Advisory Committee, is a speaker for Merck, and has received research support from MedImmune and the NIH. The rest of the authors have declared that they have no conflict of interest.


© 2011  American Academy of Allergy, Asthma & Immunology. Publié par Elsevier Masson SAS. Tous droits réservés.
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