Background: 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.
Objective: To describe the prevalence of HRV species and their associations with demographic, environmental and socioeconomic factors in healthy Aboriginal and non-Aboriginal children.
Methods: 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.
Results: 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.
Conclusions: 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.
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: firstname.lastname@example.org.
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