To understand the molecular mechanism of hemorrhagic tendency represented in hemorrhagic fever with renal syndrome (HFRS), the effect of Hantaan virus (HTNV) on the von Willebrand factor (vWF) was observed in human umbilical vein endothelial cells (HuVECs). An immunofluorescence assay (IFA) showed a significant reduction of the vWF in the cytoplasm of HTNV-infected HuVECs. The amount of vWF protein in HTNV-infected HuVECs was reduced to 86, 49, 67, and 42% of those in control HuVECs at $1^{st},;3^{rd},;5^{th},;and;7^{th}$ days of post infection (d.p.i.), respectively. However, there were no significant differences in the vWF mRNA expression in both groups at all time courses by reverse transcriptase polymerase chain reaction (RT-PCR). The amounts of secreted vWF in the culture supernatants of the HTNV-infected HuVECs were 79, 87, 83, and 82% of those in control HuVECs at $1^{st},;3^{rd},;5^{th},;and;7^{th}$ d.p.i., respectively. These results indicated that the reduction of vWF by HTNV was regulated at post-transcriptional level and this might delay the coagulation process on the site of HTNV infection, thus leading to hemorrhage in HFRS.