Pathogenesis of influenza virus-associated encephalopathy of childhood induced in animal model

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In the present study, I demonstrated that influenza virus (IFV) infection to the lungs of suckling mice enhanced encephalopathy and hypercytokinemia due to lipopolysaccharide (LPS) inoculation, and brain pathology, hypercytokinemia and absence of IFV in the brain of the animal model treated with IFV and LPS were similar to IFV-associated encephalopathy of childhood. Furthermore, it was suggested from the present study that the apoptosis of vascular endothelial cell and astrocytes causing increased permeability of blood brain barrier might be the major contributing factor forIFV-associated encephalopathy of childhood.