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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 HR C-specific antibody response is low in healthy adult sera and the 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 caps protein antigens of HRV-A, -B, and -C were tested in the plasma from nonasthmatic children (n = 47) and children presenting the emergency department with asthma exacerbations (n = 9 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 of 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. [ABSTRACT FROM AUTHOR]

Objective: To examine the influence of viral respiratory infection (VRI) on treatment response in acute asthma in children. Study design: A total of 218 children (mean age, 6.6 years) with acute asthma were recruited. Symptoms were recorded, an asthma severity score was determined, and whenever possible, a per-nasal aspirate was obtained for detection of viruses. Each child’s response to inhaled β2-agonists was assessed after 6, 12, and 24 hours. Results: The 168 children with VRI symptoms received more treatment with inhaled β2-agonists after 6 hours (P = .010), 12 hours (P = .002), and 24 hours (P = .0005) compared with the 50 children without such symptoms. Asthma severity did not differ between the 2 groups. A per-nasal aspirate was obtained from 77% of the children. The most frequently identified virus was rhinovirus (61.4%). Among children with symptoms of a VRI, those with rhinovirus had an impaired response to β2-agonists at 6 hours (P = .032). Conclusion: Children with acute asthma and symptoms of VRI respond less effectively to β2-agonists after 6, 12, or 24 hours and thus may benefit from more intense therapy and monitoring. [ABSTRACT FROM AUTHOR]

Abstract: Cysteinyl leukotrienes (cysLTs) are pro-inflammatory mediators with increasing evidence for a role in childhood acute asthma. This study examined the influence of polymorphisms in cysLT pathway genes on urinary leukotriene E4 (uLTE4) levels and clinical status in acute asthmatic children. Children aged 2–16 years were recruited during an asthma attack (n=205). Where possible, asthma severity scores were assigned, ALOX5AP G-336A, ALOX5 G-1708A, LTC4S A-444C and G-1072A, GPX4 C718T, and CYSTLTR1 T927C genotypes were determined and uLTE4 was measured in acute and convalescent samples. uLTE4 levels were higher acutely compared with convalescence (acute GM: 115.7pg/mg creatinine; 95% CI 88.6–151.1, convalescence GM: 66.4pg/mg creatinine; 95% CI 51.5–85.6; n=50 paired samples, p=0.003) and paired sample analysis showed genotype-specific effects with significantly increased uLTE4 for LTC4S-444AA (acute GM: 127.9pg/mg creatinine; 95% CI 91.8–178.3, convalescence GM: 68.2pg/mg creatinine; 95% CI 50.5–92.0; n=32, p=0.002), LTC4S-1072 GG (acute GM: 126.7pg/mg creatinine; 95% CI 95.4–168.3, convalescence GM: 78.9pg/mg creatinine; 95% CI 59.7–104.1; n=39, p=0.019) and CYSLTR1 927 TT/T_ (acute GM: 96.8pg/mg creatinine; 95% CI 73.8–126.9, convalescence GM: 62.4pg/mg creatinine; 95% CI 46.8–83.3; n=28, p=0.036) but not AC/CC, GA/AA, or TC/CC/C_, respectively. When we compared the allele frequencies of the CYSLTR1 SNP between asthmatics and non-asthmatics, the 927C allele was found to be a risk allele for asthma (OR=2.13, 95% CI: 1.06–4.26, p=0.033). Genotypes were not associated with acute or convalescent uLTE4 levels alone and neither the SNPs nor uLTE4 correlated with acute asthma severity. Leukotriene pathway gene polymorphisms may influence the magnitude of cysLT production during an attack, yet their influence alone may not be substantial enough to alter the severity of exacerbations. [Copyright &y& Elsevier]