Comparison of rhinovirus antibody titers in children with asthma exacerbations and species-specific rhinovirus infection - 27/06/14
Abstract |
Background |
Asthma exacerbations are associated with human rhinovirus (HRV) infections, and more severe exacerbations are associated with HRV-C. We have previously shown that the HRV-C–specific antibody response is low in healthy adult sera and that most of the antibody to HRV-C is cross-reactive with HRV-A.
Objectives |
To compare the antibody response to each HRV species in asthmatic and nonasthmatic children in whom the type of HRV infection was known.
Methods |
Total and specific IgG1 binding to HRV viral capsid protein antigens of HRV-A, -B, and -C were tested in the plasma from nonasthmatic children (n = 47) and children presenting to the emergency department with asthma exacerbations (n = 96). HRV, found in most of the children at the time of their exacerbation (72%), was analyzed using molecular typing.
Results |
Asthmatic children had higher antibody responses to HRV. The titers specific to HRV-A, and to a lesser extent HRV-B, were higher than in nonasthmatic controls. The species-specific responses to HRV-C were markedly lower than titers to HRV-A and HRV-B in both asthmatic and nonasthmatic children (P < .001). The titers both at presentation and after convalescence were not associated with the HRV genotype detected during the exacerbation.
Conclusions |
The higher total anti-HRV antibody titers of asthmatic children and their higher anti–HRV-A and -B titers show their development of a heightened antiviral immune response. The low species-specific HRV-C titers found in all groups, even when the virus was found, point to a different and possibly less efficacious immune response to this species.
Le texte complet de cet article est disponible en PDF.Key words : Human rhinovirus, VP1, IgG1 antibody, asthma exacerbation, children
Abbreviations used : E30, ED, GST, HPV, HRV, VP1
Plan
| This work was supported by the National Health and Medical Research Council of Australia. J.I. was supported by an Australian Postgraduate Award, a University of Western Australia Scholarship, a Stan and Jean Perron Scholarship, and an Asthma Foundation of Western Australia Scholarship. |
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| Disclosure of potential conflict of interest: J. Iwasaki has received research support from the National Health and Medical Research Council of Australia, has received travel support from Asthma Foundation WA, Friends of the Institute for Child Health Research, the Australian Postgraduate Award, the European Academy of Allergy and Clinical Immunology, and the Stan and Jean Perron Scholarship. S.-K. Khoo has received research support from the National Health and Medical Research Council of Australia and the University of Western Australia and is employed by the University of Western Australia. J. Bizzintino and I. A. Laing have received research support from the National Health and Medical Research Council of Australia and are employed by the University of Western Australia. G. Zhang has received research support from Brightspark. D. W. Cox has received research support from the National Health and Medical Research Council of Australia. P. N. Le Souëf has received research support from the National Health and Medical Research Council of Australia; is on advisory boards for Teva and GlaxoSmithKline; is employed by the University of Western Australia; and has received payment for lectures from GlaxoSmithKline Saudi Arabia. W. R. Thomas has received research support from the National Health and Medical Research Council of Australia; has received writing assistance, medicines, equipment, or administrative support from the Health Department of Western Australia; and has received royalties for use of allergen patents. B. J. Hales has received research support from the National Health and Medical Research Council of Australia and is employed by the Telethon Institute for Child Health Research. W.-A. Smith declares no relevant conflicts of interest. |
Vol 134 - N° 1
P. 25 - juillet 2014 Retour au numéro
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