The burden of respiratory viral disease in hospitalized children in Paris

Department of Pediatrics and Emergency, University Paris 5, Saint Vincent de Paul APHP Hospital, 75014, Paris, France.
European Journal of Pediatrics (Impact Factor: 1.89). 05/2008; 167(4):435-6. DOI: 10.1007/s00431-007-0529-5
Source: PubMed


A virus was identified in 464 out of 1,212 patients, 8 days to 16 years of age, who were admitted to the hospital in Paris during a 3 year period. Respiratory syncytial virus (RSV) was found in 428 patients, 74% were younger than 6 months with bronchiolitis, and 6% were older than 2 years. RSV was the first virus isolated in all patients and in those with pneumonia or asthma. The low number of admissions due to parainfluenzae viruses is characteristic of this area compared to other countries.

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    ABSTRACT: Respiratory syncytial virus (RSV) is the leading cause of infant bronchiolitis. The closely related pneumonia virus of mice (PVM) causes a similar immune-mediated disease in mice, which allows an analysis of host factors that lead to severe illness. This project was designed to compare the immune responses to lethal and sublethal doses of PVM strain 15 in Balb/c and C57Bl/6 mice. Balb/c mice responded to PVM infection with an earlier and stronger innate response that failed to control viral replication. Production of inflammatory cyto- and chemokines, as well as infiltration of neutrophils and IFN-γ secreting natural killer cells into the lungs, was more predominant in Balb/c mice. In contrast, C57Bl/6 mice were capable of suppressing both viral replication and innate inflammatory responses. After a sublethal infection, PVM-induced IFN-γ production by splenocytes was stronger early during infection and weaker at late time points in C57Bl/6 mice when compared to Balb/c mice. Furthermore, although the IgG levels were similar and the mucosal IgA titres lower, the virus neutralizing antibody titres were higher in C57Bl/6 mice than in Balb/c mice. Overall, the difference in susceptibility of these two strains appeared to be related not to an inherent T helper bias, but to the capacity of the C57Bl/6 mice to control both viral replication and the immune response elicited by PVM.
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