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Objective: To establish a liver injury model in BALB/c nude mice infected with murine cytomegalovirus (MCMV). Methods: 10 healthy SPF BALB/c nude mice were randomly divided into experimental group and control group, each group 5. The mice in the experimental group were intraperitoneally inoculated with 250 μL MCMV virus suspension, and the mice in control group were intraperitoneally inoculated with 250 μL DMEM culture medium, the mice were sacrificed 7 days after inoculation, and their livers were aseptically separated. The liver tissue damage of nude mice was observed by measuring alanine aminotransferase (ALT) in liver tissue, real-time fluorescence quantitative PCR for detection MCMV DNA copy number and hematoxylin-eosin (HE) staining and other methods. Results: Nude mice in all the experimental groups showed ascites to varying degrees. ALT value in liver tissue of nude mice in experimental group was significantly higher than that in control group (P<0.05). Real-time fluorescence quantitative PCR detected that Liver MCMV DNA of nude mice in the experimental group was positive. HE staining of pathological sections of liver in the experimental group showed a large number of inflammatory cell infiltration, eosinophilic changes of liver cells, and irregular inclusion bodies, while the control group was normal. Conclusion: The liver injury model of nude mice is successfully established after intraperitoneal injection of 250 μL MCMV suspension for 7 days, which provided a beneficial condition for the study of the pathogenesis of human cytometomethovirus (HCMV) and the research and development of antiviral drugs and vaccines. [ABSTRACT FROM AUTHOR]

Objective: To establish the activation of latent murine cytomegalovirus and analyze the schedule of activation; To confirm the transcription of MCMV immediate early protein 1(ie1) gene and complete the kinetics of transcription of ie1 gene and production of virus; To set up an activation model of latent MCMV for further research of the types of the cells where MCMV chromosome maintains during the period of latency. Methods: 2 days after birth, 500 PFU/5 μL of MCMV of minimum essential medium was injected into the right cerebral hemisphere of neonatal BALB/c mice. Control mice were similarly injected with minimum essential medium for 16 weeks. Intracranial injection and intraperitoneal injection of 15 μg/kg weight lipopolysaccharide(LPS) were administered, and saline was injected as a contrast. At 1, 2, 5, 7, 14 and 21 days postinfection, five mice from two groups were killed and the brains were removed. The brains were used for reverse transcriptase-polymerase chain reaction(RT-PCR) assays and sensitive plaque assays(combined plaque with RT-PCR) to detect the IE1 mRNA and virus titer. Results: IE1 mRNA was detected at 14 and 21 days in the group LPS. Cytopathic effect(CPE)was detected at 14 and 21 days, and titer were approximately 4.29×104 PFU/μL and 5.20×105 PFU/μL. Transcription of IE1 mRNA was detected at 7, 14 and 21 days in the homogenate of mouse embryonic fibroblasts(MEFs)by sensitive plaque assays. Conclusions: The activation model of latent MCMV was established, ie1 mRNA was detected and the schedule of it during the period of activation. The model would be provided in further research of MCMV latency and activation in brains. It could also provide basis for the research of human cytomegalovirus(HCMV). [ABSTRACT FROM AUTHOR]