动物造模,Cox A16型手足口病 z-bio 2023-05-04 359

　　Objective To establish a 3-day-old BALB/c suckling mouse model of CoxA16 hand foot mouth disease (HFMD), and to study its immunology and pathology.

　　Methods Three day old BALB/c suckling mice were intraperitoneally injected with Cox A16 strain, and their 50% lethal dose (LD50) was measured. Their 14 day survival days and clinical symptom scores were observed. The 3LD50 virus was used to attack the virus, and the infection degree, weight change, and number of deaths within 14 days were observed. The average survival days and mortality were calculated. The samples were taken when the onset reached the peak on the sixth day of infection. The serum MCP-1 and MIP-1 were detected by CBA method α、 The content of G-CSF was detected by real-time fluorescence quantitative RT-PCR to detect the viral load in the muscle tissue, heart, brain and intestine of the hind limb, and the pathological changes in the muscle and brain of the hind limb were observed by HE staining.

　　Results Three day old BALB/c suckling mice infected with Cox A16 strain showed decreased activity, hind limb paralysis, weight loss and death. The virulence of Cox A16 strain was 56 LD50 per milliliter. Within 14 days after infection, compared with the normal control group, the survival days, mortality, clinical infection score and body weight of suckling rats in the model group were significantly different (P<0.01). On the 6th day after infection, the levels of MCP-1 and G-CSF in serum increased significantly (P<0.01). The viral load of muscle tissue, heart, brain and intestine of hind limb was significantly higher than that of normal group (P<0.01), and the viral load of muscle tissue of hind limb was the highest. Pathological observation of HE staining showed that there was a large area of atrophy and inflammation in the muscle tissue of the hind limb, and there was atrophy of nerve cells in the brain tissue to varying degrees.

　　Conclusion A 3-day old BALB/c suckling mouse model of CoxA16 HFMD was successfully established, which lays a foundation for drug evaluation and mechanism study of COX A16 HFMD.