OBJECTIVE: To establish a mouse model using a mouse adapted strain of seasonal influenza virus H3N2 and to explain the molecular mechanism of the pathogenicity of the adapted strain. Method: A/Aichi/2/68 (H3N2) (WT) is more abundant in mice. After the second indication, a mouse-adapted strain (MA-7) was obtained, and MA-7 was in BALB/c mice In the nose. Establish an infected mouse model, and analyze the indicated strains based on clinical symptoms, weight loss rate, virus replication, histopathology and other 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. All mice died within 9 days after MA-7 infection, and the weight loss rate exceeded 30%. Can virus replication be detected, the titer of lung tissue is as high as 105.5TCID50, and is there interstitial pneumonia? Does genetic comparison show that MA-7 has five mutations in HA, NA, PA and NP genes?
Conclusion: We have successfully established a H3N2 adaptive strain mouse model. It 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 indicator strain is related to the 5 mutation sites?