Abnormal expressions of inflammatory-related mediators and inhibition of fat metabolism in mice infected with influenza a virus

The pathophysiological role of influenza infection is poorly understood. in this study,one non-neurovirulent virus (iav/aichi/2/68/h3n2) strain was used to infect intra-nasally mice at different age to investigate the mechanism of cerebral edema formation and lower activities of mitochondria enzymes after influenza a virus (iav) infection. mice suffered 46.4% mortality in newborn compared with 96.0% in weanling,100% in adult on day 7,respectively. iav-rna was easily detected in the brain of newborn mice. significant production of endothelin-1 and inducible nitric oxide syntheses were increased on the 3rd and 5th day after iav infection,associated with increasing blood-brain barrier permeability,brain edema formation and the higher mortality of animals. production of tumor necrosis factor-α was related to inhibition of mitochondrial enzyme activities,suggesting that over expression of inflammatory cytokines and lower enzyme activities in mitochondria after iav infection.