动物造模 z-bio 2022-08-29 282

　　OBJECTIVE: To establish a mouse model with the seasonal influenza virus H3N2 mouse-adapted strain, and to describe the molecular mechanism of the adaptation to the change of the virulence of the strain.

　　METHODS: A/Aichi/2/68(H3N2)(WT) was adapted for multiple times in mice to obtain a mouse-adapted strain (MA-7). MA-7 infected BALB/c mice nasally. According to clinical symptoms and weight loss Key indicators such as virus replication rate, virus replication and histopathology were used to determine the establishment of a mouse model, and to analyze the molecular mechanism of adapting to changes in the pathogenicity of the strain.

　　Results: Mice infected with WT had 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%. The degree of TCID50 was as high as 105.5 TCID50 and interstitial pneumonia occurred. Gene alignment revealed that MA-7 had 5 mutations in HA, NA, PA and NP genes.

　　Conclusion: The H3N2-adapted strain mouse model was successfully established, which can be used to study the pathogenesis of H3N2 influenza virus and its drug, vaccine, antibody evaluation, etc. The enhanced pathogenicity of the adapted strain may be related to five mutation sites.