Objective: To establish a mouse model with the seasonal influenza virus H3N2 mouse adaptation strain, and to explain the molecular mechanism of the change in the pathogenicity of the adaptation strain
Methods: A/Aichi/2/68 (H3N2) (WT
Results: The mice infected with WT had no obvious symptoms and no virus replication was detected. All the mice died within 9 days after MA-7 infection, with a weight loss rate of more than 30%. Virus replication could be detected in multiple tissues, and the titer in lung tissues was up to 105.5 TCID50 and interstitial pneumonia appeared. Gene comparison showed that MA-7 had mutations in 5 loci of HA, NA, PA and NP genes
Conclusion: A mouse model of H3N2 adaptive strain has been successfully established, which can be used to study the pathogenesis of H3N2 influenza virus and the evaluation of its drugs, vaccines and antibodies. The increased pathogenicity of the adaptive strain may be related to five mutation sites