Human cytomegalovirus (HCMV) infections are among the most common community acquired infections. More than 70 percent of the adult population are carriers of HCMV antibodies. As a member of the herpesviridae family, HCMV remains latent in the body after a primary infection. HCMV may cause life threatening infections in immunocompromised patients. The pathogenesis of a HCMV infection is complex. Organ damage is due to a combination of immunologic and viral cell damage. Endothelial cells, monocytes and neutrofil granulocytes play a key role in the pathogenesis. The HCMV coded receptor US28 has the ability to bind chemokines. Among them are the C-C chemokine MCP-1 and the CX3C chemokine fractalkine. Of these two, fractalkine is bound with the highest affinity. Endothelial cells have the ability to express these chemokines. Our hypothesis is that the binding of fractalkine and MCP-1 to the US28 receptor, may contribute to the transmission of HCMV from leucocytes to endothelial cells. This student project’s objective was to study in what extent endothelial cells express MCP-1 and fractalkine under normal conditions, and after activation. We also studied whether a HCMV infection would change the expression or release of MCP-1 and fractalkine. In this project we used ELISA-technique, flow cytometri and PCR to detect expression and release of the two chemokines.