CYTOMEGALOVIRUS-INFECTION AMPLIFIES CLASS-I MAJOR HISTOCOMPATIBILITY COMPLEX EXPRESSION ON CULTURED HUMAN ENDOTHELIAL-CELLS

Cytomegalovirus infection, a common complication in immunosuppressed g raft recipients, bears an adverse impact on graft survival. Cytomegalo virus enhances the expression of the monotypic determinants of the cla ss I major histocompatibility complex molecule by the endothelium, pos sibly rendering the endothelial cells more immunogenic and prone to at tack by the allogeneic lymphocytes. In the present study, we focused o n the effect of cytomegalovirus on the endothelial cell expression of different class I genes, on the relation between the extent of endothe lial cell infection and the class I effect, and on the time course of the class I changes induced by the cytomegalovirus infection. Cytomega lovirus infection of primary cultures of human umbilical vein endothel ial cells augmented the expression of the A2, A3, and B7 class I major histocompatibility complex genes when compared with uninfected cells. beta2 microglobulin upregulation by the infected cells paralleled the changes in specific class I expression; this effect was significant o nly after 7 days after infection. Double immunocytochemical staining a nd fluorescence-activated cell sorter analysis revealed that the class I enhancement was uniform throughout the umbilical vein endothelial c ell monolayer and not restricted to the cells that expressed cytomegal ovirus early or late antigens. Ultraviolet-inactivated supernatants fr om infected umbilical vein endothelial cell did not increase class I e xpression on uninfected cells. In conclusion, cytomegalovirus might af fect graft survival by amplifying the changes in class I expression be yond the sites of viral replication.