Aim: This study aimed to explore the potential role of IL-17 in the pathological damage to the salivary gland during CMV infection. Materials & methods: For all studies, 4-week-old female BALB/c mice were used. Mouse embryo fibroblast cells were isolated from embryos of pregnant mice. The Smith murine CMV (MCMV) strain was propagated and obtained from homogenates of the salivary glands. BALB/c mice were randomly divided into two groups. Mice in one group were infected with Smith MCMV to establish disseminated infection; mice in the other group were controls. Four mice of each group were randomly chosen to be harvested on days 3, 7, 14 and 28. Viral titers in salivary gland tissues were determined using a standard plaque assay; IL-17(+) T cells in the spleen were analyzed by flow cytometry; the expressions of IL-17 and IL-17 receptor (IL-17R) mRNA was measured by reverse transcription PCR; and the pathology of the salivary glands in infected mice were assessed by hematoxylin and eosin staining. Results: The viral titers in salivary gland tissues, which were much higher than those of other organs, elevated on day 7 and peaked on day 14, then gradually declined on day 28. The percentages of CD4(+)IL-17(+) T cells were increased in MCMV-infected mice compared with controls, with the main increase of CD4(+)IL-17(+) T cells being Th17 cells (p < 0.05). In salivary gland tissues, the expression of IL-17 and IL-17R mRNA increased significantly and achieved the highest level on day 14, which was significantly higher than that of the controls (p < 0.05). Compared with controls, serious inflammatory cellular infiltrates in the salivary glands were present on day 7 after MCMV infection, and on day 14, many of the cellular infiltrate became larger and coalesced with neighboring foci. We found that IL-17 and IL-17R were enriched in the salivary glands when the tissues were mainly injured. Conclusion: The results illustrated that the inflammatory factors, IL-17 and IL-17R, possibly contributed to the process of viral infection and played a part in inducing pathological damage of the salivary gland.