Rhinovirus-C detection in children presenting with acute respiratory infection to hospital in Brazil.

Human rhinovirus (RV) is a common cause of acute respiratory infection (ARI) in children. We aimed to characterize the clinical and demographic features associated with different RV species detected in children attending hospital with ARI, from low-income families in North-east Brazil. Nasopharyngeal aspirates were collected from 630 children <5 years with ARI. Clinical diagnosis and disease severity were also recorded. Samples were analyzed by multiplex PCR for 18 viral and atypical bacterial pathogens; RV positive samples underwent partial sequencing to determine species and type. RV was the fourth commonest pathogen accounting for 18.7% of pathogens detected. RV was commonly detected in children with bronchiolitis, pneumonia, and asthma/episodic viral wheeze (EVW). Species and type were assigned in 112 cases (73% RV-A; 27% RV-C; 0% RV-B). Generally, there were no differences in clinical or demographic characteristics between those infected with RV-A and RV-C. However, in children with asthma/EVW, RV-C was detected relatively more frequently than RV-A (23% vs. 5%; P = 0.04). Our findings highlight RV as a potentially important pathogen in this setting. Generally, clinical and demographic features were similar in children in whom RV-A and C species were detected. However, RV-C was more frequently found in children with asthma/EVW than RV-A.

Symptomatic viral infection is associated with impaired response to treatment in children with acute asthma.

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 ß(2)-agonists was assessed after 6, 12, and 24 hours. RESULTS: The 168 children with VRI symptoms received more treatment with inhaled ß(2)-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 ß(2)-agonists at 6 hours (P = .032). CONCLUSION: Children with acute asthma and symptoms of VRI respond less effectively to ß(2)-agonists after 6, 12, or 24 hours and thus may benefit from more intense therapy and monitoring.

The role of parasites in genetic susceptibility to allergy: IgE, helminthic infection and allergy, and the evolution of the human immune system.

There have been numerous studies in the mouse illustrating the dichotomy of T cell responses, with the common classification orchestrated around Th1 vs. Th2 responses. This classification is now widely applied to human disease as well and the generic conclusion is that the Th1 responses are more likely to occur secondary to specific microbiologic insult but also inflammatory responses. In contrast, the Th2 response is the prevalent response in subjects with atopy and allergic disease but is also the mechanism for protection against helminthic infections. Unfortunately, the paradigm of Th1 vs. Th2 is not as clear in the human as it is in mouse models. Even so, the immunological mechanisms responsible for IgE production that are protective in helminthic infections, i.e. Schistosoma, are similar to those for the production of specific IgE against allergens. In fact, there also appear to be associations in the memory T cell subpopulation CD4+CD45RO+ and the elicitation of IgE against both parasites and allergens. In this review, we present the overall contemporary scheme on the role of parasites in genetic susceptibility to allergic IgE, helminthic infections with specific discussion of its implications for the evolution of the human immune system.