Aim To explore the mechanisms of influenza virus infection in the formation of atherosclerosis from the cellular and molecular levels through investigating amount of intercellular adhesion molecule-1and vascular cell adhesion molecule-1after human umbilical vein endothelial cell was infected by influenza virus. Methods SYBR Green reverse transcription polymerase chain reaction(RT-PCR),flow cytometry and enzyme-linked immunosorbent assay were used to detect the timing expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 of human umbilical vein endothelial cells infected by influenza virus at 0 h,24 h,48 h and 72 h. Results Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1were measured by these three methods after human umbilical vein endothelial cell was infected by influenza virus.The base level of the two inflammatory factors was expressed at a low level at 0 h,and began to increase after influenza virus infection,reached the peak at 24 h.After 48 h,it declined obviously and remained a relatively high level at 72 h.The amount of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in the infected groups was higher than that in the control group(P﹤0.05). Conclusion This study showed that influenza virus infection could increase the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1,and then influenza virus infection might lead to dysfunction of vascular endothelial cells and involve in the inflammatory response of atherosclerosis.