流感病毒H3N2鼠适应株 z-bo 2020-12-08 407

　　Purpose: 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. Methods: A/Aichi/2/68 (H3N2) (WT) was adapted to mice for multiple times to obtain a murine adapted strain (MA-7). MA-7 was nasally infected with BALB/c mice, according to clinical symptoms and weight loss Key indicators such as virus replication and histopathology determine the establishment of the mouse model, and analyze the molecular mechanism of adapting to changes in the pathogenicity of the strain. Results: The mice were infected with WT without 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%. Virus replication was detected in multiple tissues, and the lung tissue was dripping. The degree is as high as 105.5 TCID50 and interstitial pneumonia appears. Gene comparison revealed that MA-7 has 5 mutations in HA, NA, PA and NP genes.

　　 Conclusion: The H3N2 adapted strain mouse model has been successfully established, which can be used to study the pathogenesis of H3N2 influenza virus and its drugs, vaccines, antibody evaluation, etc. The increased pathogenicity of the adapted strain may be related to 5 mutation sites.