Studies On The Pathogenesis And Immunological Of Bovine Respiratory Syncytial Virus In Mice

Bovine respiratory syncytial disease caused by an acute febrile respiratory diseases. Since1967BRSV isolated for the first time in Switzerland, have an outbreak of the disease in manydeveloped countries of the bovine industry. At present, the domestic bovine respiratory syncytialdisease mainly in the separation and identification of the virus, viral antigen detection, serologicalmethods and molecular biology to detect, but the characteristics of bovine and experimentalanimal models of pathogenicity and immune,The study has yet to see the relevant reports.To further study bovine respiratory syncytial virus pathogenicity and immune characteristicsof the experimental study commonly used laboratory animals in biomedical research Kunmingmice were used as research subjects, instead of the more difficult to carry out experimentalenvironmental conditions control cattle.Kunming mice pathogenicity experimental, BRSV intranasal inoculation (TCID5.75010-/100μL)6to9-week-old Kunming mice were observed and recorded clinical symptoms, take the lungs andtrachea tissue by virus isolation, infectious titer determination, RT-PCR was used to detect thehistopathology confirmed the pathogenicity of the virus in mice. The results, after challengingcompared to the control group, mental fatigue, weight loss, respiratory to accelerate, atrophy of agroup, severe abdominal breathing; lungs and trachea tissue supernatant MDBK cells can produceCPE, lung tissue TCID50titers above the trachea tissue; target fragment detected by RT-PCR frominfected lung tissue of mice; pathological tissue changes the mice bronchial lumen serous exudatebronchial wall due to congestion, edema and leukocyte infiltration and become swollen andthickened alveolar cavity filled with serous, mixed with a small amount of neutrophils, red bloodcells and the shedding of epithelial cells, widening of the alveolar septa, the capillaries flat,congestion, edema mainly interstitial pneumonia.The BRSV-HJ in Kunming mice immune model test, separating the strains inactivated withformaldehyde, preparation of Freund’s adjuvant inactivated antigen by intranasal mucosa,subcutaneous different immune pathways Kunming mice inoculation. Taken under sterileconditions after two free mouse spleen lymphocytes were separated lymphocyte proliferationassays.14days after the challenged, lung and serum neutralization test taken after the challenge,ELISA was used to detect the mouse lung and serum IgG, IgA, lymphocyte the Th1/Th2subsetsrelated cytokines IFN-γ, IL-5secretion. Lymphocyte proliferation test results: two free realresults show that enhanced T lymphocyte proliferation, immune and control groups showedsignificant differences (P <0.05). Anti-BRSV IgG, IgA, and antibodies produced in mouse lungsand serum. Wherein the serum anti-BRSV IgG highest value reached1:12000, IgA highest value1:5000, neutralizing antibody1:20, the lungs of IgG highest value reached1:2000, IgA highestvalue of1:500, and the antibody1:6. Each immunohistochemistry lungs and lymphocyte secretionof IFN-γ and IL-5secretion and control group, serum IFN-γ, IL-5secretion and the control groupcompared to the difference was not significant difference (P<0.05); significant (P>0.05).Conclusion: BRSV Freund’s adjuvant inactivated antigen intranasal immunization6to9-week-old Kunming mice in serum and lung to produce antibody titers induced mucosal immunity, cellularimmunity and humoral immunity, reducing the virus in mice replication and proliferation of thebody has a protective effect on mice.Bovine respiratory syncytial virus Kunming mice pathogenicity and the establishment ofimmune model can provide a reference for future indepth study of virus pathogenicity andimmunology research on the body of animals and the reference.