Objective To investigate the mechanism of HCV infection in the pathogenesis of atherosclerosis with a model of human umbilical vein endothelial cells (HUVECs) stimulated by HCV in vitro. Methods HUVECs were stimulated with 1. 0 MOI HCVcc for 48 hours.CCK8 assay was used to measure cell proliferation; flow cytometry was used to measure cell apoptosis and cell cycle; wound healing assay and monocyte-endothelial adhesion assay were used to evaluate the influence of HCV on the migration and adhesion of HUVECs; quantitative real-time PCR and Western blot were used to measure the expression of inflammatory factors and endothelial injury factors in HUVECs stimulated by HCV. The two-independent-samples t test was used for comparison between two groups; an analysis of variance was used for comparison between multiple groups, and the LSD-t test was used for further comparison between two groups. Results Compared with the control group, the HCV group had no significant changes in the growth, apoptosis, and cell cycle of HUVECs (all P > 0. 05) . HCV stimulation inhibited the migration of HUVECs and enhanced their adhesion ability. Compared with the control group, the HCV group had significant increases in the mRNA and protein expression of the inflammatory factors interleukin-6 and interleukin-1β and the chemokines CXCL10 and monocyte chemotactic protein 1 (mRNA expression: t =-10. 155, -12. 048, -5. 025, and-20. 116, all P < 0. 05; protein expression: F = 2541. 739, 4806. 490, 477. 608, and 501. 38, all P < 0. 001) . HCV stimulation significantly upregulated the expression of the endothelial injury factors endothelin-1 and vascular endothelial growth factor and the adhesion molecules intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in HUVECs (t =-4. 530, -4. 497, -7. 692, and-7. 449, all P < 0. 05) . Conclusion HCV can cause inflammatory changes and dysfunction in endothelial cells and thus affect the development of atherosclerosis.