Abstract: Objective To explore the expression and possible mechanism of survivin protein in viral myocarditis (VMC). Methods The VMC cell model was created by infecting primary cardiac myocyte with Coxsackie virus (CVB3) in SD neonatal rats. Morphology and pulsation of myocardial cells were observed at 0, 12, 24, 36, 48, 60 hours after infected by CVBs. The degree of injury of myocardial cells was evaluated by lactic dehydrogenase (LDH) enzyme release test. Cell apoptosis was assessed by flow cytometry (FCM). And the expression levels of survivin protein and Cleaved-caspase-3 were detected by Western blot. Results At 48 hours after infected by CVB3, primary myocardial cells in neonatal rat were observed to gradually shrink and became round, and simultaneously, the beating rate was decreased and became irregular. At 60 hours after infected, most cells stopped beating, dropped off from the cell wall, and were dissolved. The cell apoptosis reached the peak (35.85%±3.76%) at 60 hours after infected. The expression of survivin protein was significantly increased after infected, and reached the peak (1.88± 0.39) at 12 hours after infected, which was 1.88 times higher than control group. After that, the expression of survivin protein was decreased and reached its minimum value (0.47±0.41) at 60 hours after infected. The expression of cleaved-caspase-3 was also elevated after infected, and reached the peak at 60 hours (3.46±0.16) after infected. The expression of surviving protein in myocardial cells were negatively correlated with cell apoptosis and the expression of cleaved-caspase-3 (r = －0.727, －0.677, P all < 0.01). Conclusion The expression of survivin protein increases in VMC, which may be involved in the anti-myocardial apoptosis at early stage.