Purpose: Use the seasonal influenza virus H3N2 mouse adaptive strain to establish a mouse model and explain the molecular mechanism of the pathogenic changes of the adaptive strain?
"Method: A/Aichi/2/68(H3N2) (WT) is more abundant in mice. After the second adaptation, a mouse-adapted strain (MA-7) was obtained, and MA-7 nose paired BALB/c mice. Infected from. Establish a mouse model, and use the clinical symptoms, weight loss rate, virus replication and histopathological analysis of indicator strains as important indicators. The molecular mechanism of pathogenic changes?
Result: After infecting mice with WT, there were no obvious symptoms and no virus replication was detected. After MA-7 infection, all mice died within 9 days and lost more than 30 weights. Is virus replication detected, lung tissue titer is as high as 105.5TCID50, and interstitial pneumonia appears? Genetic comparison shows that MA-7 contains 5. Mutations in HA, NA, PA and P genes?
Conclusion: We have successfully established a mouse model of H3N2 influenza virus, which can be used to study the etiology of H3N2 influenza virus and its drugs, vaccines, antibody evaluation, etc. Is it possible that the increased pathogenicity of the indicated strain is related to the 5 mutation sites?