Please cite this paper as: Esposito et al. (2012) Impact of viral infections in children with community‐acquired pneumonia: results of a study of 17 respiratory viruses. Influenza and Other Respiratory Viruses DOI: 10.1111/j.1750‐2659.2012.00340.x. Background  Little is known about the prevalence of viral infections in children with community‐acquired pneumonia (CAP). Objectives  To describe the clinical and virological data collected from children with radiographically confirmed CAP in whom 17 respiratory viruses were sought in respiratory secretion samples during the acute phase of the disease. Patients and methods  The study involved 592 children with radiographically confirmed CAP whose respiratory secretion samples were tested using the Luminex xTAG Respiratory Virus Panel Fast assay, which simultaneously detects influenza A virus, influenza B virus, respiratory syncytial virus (RSV)‐A and ‐B, parainfluenzavirus‐1, ‐2, ‐3, and ‐4, adenovirus, human metapneumovirus, coronaviruses 229E, NL63, OC43, and HKU1, enterovirus/rhinovirus, and bocavirus. A real‐time PCR assay was used to identify the rhinovirus in the enterovirus/rhinovirus‐positive samples. Results  A total of 435 children (73·5%) were positive for at least one virus: the most frequently detected was RSV, which was found in 188 (31·7%), followed by rhinovirus (n = 144, 24·3%), bocavirus (n = 60, 10·1%), influenza viruses (n = 57, 9·6), and hMPV (n = 49, 8·2%). Viral co‐infections were found in 117 children (19·7% of the enrolled children; 26·9% of those with viral infections). Marginal differences were found between the infections owing to a single virus. Co‐infections showed radiographic evidence of alveolar pneumonia significantly more frequently than single infections (OR 1·72, 95% CI 1·05–2·81). Conclusions  The findings of this study highlight the importance of respiratory viruses (mainly RSV and rhinovirus) in children with CAP and show the characteristics of both the single infections and co‐infections associated with the disease.

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It has been shown that chronic treatment with lithium carbonate (Li(2)CO(3)) in presymptomatic SOD1G93A transgenic male mice, a model of ALS, was able to remarkably increase their lifespan through the activation of autophagy and the promotion of mitochondriogenesis and neurogenesis. This prompted us to test the lithium effect also in female SOD1G93A mice with two phenotypes of different disease severity. Female SOD1G93A mice of C57BL/6J or 129S2/Sv genetic background were treated daily with Li(2)CO(3) 37 mg/kg (1 mEq/kg) i.p. starting from age 75 days until death. Grip strength, latency to fall on rotarod and body weight were monitored twice weekly. At the time of death the spinal cord was removed to assess the number of motor neurons and to measure the expression of a marker of autophagy (LCII) and the activity of mitochondrial complex IV. We observed a significant anticipation of the onset and reduced survival in 129Sv/G93A and no effect in C57/G93A mice treated with lithium compared to vehicle treated mice. Moreover, lithium neither exerted neuroprotective effects nor increased the expression of LCII and the activity of mitochondrial complex IV in the spinal cord. The present study does not identify any therapeutic or neuroprotective effect of lithium in SOD1G93A female mice.