(1) Replication method Take out suckling mice born 1 to 3 days after birth, and inoculate the brain with 0.02 ml C6/36DEN-2 cell virus with a TCID50 of 10-4. Histopathological observation under an optical microscope showed that there was a small amount of local or spot hemorrhage under the companion and brain parenchyma, telangiectasia, congestion, perivascular inflammatory cell infiltration, local hemorrhage in the brain tissue, and showed submucosal hemorrhage; in the alveoli Septum enlargement, hepatocyte edema, steatosis, hepatic macrophage proliferation and hypertrophy, hepatic sinusoid dilatation and congestion. Electron microscope observation showed that vascular endothelial cells were degenerated in vacuoles and primary lysosomes. Neurogenic and glial cells had mild mitochondria and formed vacuoles in the cells.
(2) Model characteristics Dengue fever virus can cause brain tissue damage in young mice, which is manifested by inflammatory changes and hemorrhage in the brain tissue. In addition to dilation and congestion, vascular endothelial cell degeneration, necrosis and red blood cell extravasation, cerebrovascular disease. Blood vessel bleeding and damage are related to the pathogenicity of the virus.
(3) Comparative Medicine Dengue fever virus infection in lactating mice can cause severe pathological changes in the brain tissue of lactating mice. This pathological feature is similar to the clinicopathological changes of human dengue hemorrhagic fever and dengue shock syndrome. In lactating mice infected with DFV, this model is of great value for studying the etiology of dengue virus infection.