Human rhinovirus (HRV) species C (HRV-C) have been associated with frequent and severe acute lower respiratory infections and asthma in hospitalized children. The prevalence of HRV-C among healthy children and whether this varies with ethnicity is unknown.
To describe the prevalence of HRV species and their associations with demographic, environmental and socioeconomic factors in healthy Aboriginal and non-Aboriginal children.
Respiratory viruses and bacteria were identified in 1006 nasopharyngeal aspirates collected from a cohort of 79 Aboriginal and 88 non-Aboriginal Western Australian children before 2 years of age. HRV-positive nasopharyngeal aspirates were typed for HRV species and genotypes. Longitudinal growth models incorporating generalized estimating equations were used to investigate associations between HRV species and potential risk factors.
Of the 159 typed specimens, we identified 83 (52.2%) human rhinovirus species A (HRV-A), 26 (16.4%), human rhinovirus species B and 50 (31.4%) HRV-C. HRV-C was associated with upper respiratory symptoms in Aboriginal (odds ratio, 3.77; 95% confidence interval:1.05–13.55) and non-Aboriginal children (odds ratio, 5.85; 95% confidence interval: 2.33–14.66). HRV-A and HRV-C were associated with carriage of respiratory bacteria. In Aboriginal children, HRV-A was more common in the summer and in those whose mothers were employed prior to delivery. In non-Aboriginal children, day-care attendance and exclusive breast-feeding at age 6–8 weeks were associated with detection of HRV-A, and gestational smoking with detection of HRV-C.
Factors associated with the presence of HRV differ between Aboriginal and non-Aboriginal children. In contrast to HRV-A, HRV-C is associated with upper respiratory symptoms suggesting that HRV-C is likely to be implicated in respiratory illness.
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From the *School of Paediatrics and Child Health, The University of Western Australia, Perth, Australia; †Telethon Institute for Child Health Research, Centre for Child Health Research, The University of Western Australia, Perth, Australia; ‡Division of Microbiology and Infectious Diseases, PathWest Laboratory Medicine, Perth, Australia; §School of Pathology and Laboratory Medicine, The University of Western Australia, Perth, Australia; and ¶University of Wisconsin-Madison, Madison, WI.
Accepted for publication March 1, 2012.
This study was funded through the National Health and Medical Research Council Project Grant #212044 and two Healthway Grants (#6028 and #10564). The authors have no other funding or conflicts of interest to disclose.
Address for correspondence: Alicia Annamalay, BMedSci (Hons), School of Paediatrics and Child Health, University Of Western Australia, Perth, Australia. E-mail: email@example.com.
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