THE HUMAN POLYOMAVIRUS, JCV, DOES NOT SHARE RECEPTOR SPECIFICITY WITHSV40 ON HUMAN GLIAL-CELLS

The initial event in the life cycle of a virus is its interaction with specific receptors present on the surface of a cell. Understanding th ese interactions is important to our understanding of viral tropism an d tissue specific pathology associated with viral disease. The human p olyomavirus, JCV, is the etiological agent of the fatal central nervou s system (CNS) demyelinating disease, progressive multifocal leukoence phalopathy (PML). PML is the direct result of ICV infection of oligode ndrocytes, the myelin producing cell in the CNS. In vivo, JCV can be d etected in oligodendrocytes, astrocytes, lymphoid tissue, and peripher al blood of PML patients. In vitro, JCV infects human glial cells, ton silar stromal cells, and, to a limited extent human B lymphocytes. The initial step in infection of cells by JCV is at the level of attachme nt and entry. A specific cell surface receptor for JCV on human glial cells has not been identified. To begin to understand the nature of JC V receptors on human glial cells, large quantities of a previously cha racterized hybrid JC virus (Mad-1/SVE Delta) were purified, A direct v irus binding assay demonstrated that these highly purified and labeled JCV virions bound to a finite number of cellular receptors on human g lial cells. A competitive virus binding assay demonstrated that an exc ess of unlabeled JCV competed with labeled JCV more efficiently than d id an excess of purified SV40. Furthermore, anti-class I antibodies wh ich inhibited infection of glial cells by SV40 had no significant effe ct on infection by JCV These results imply that JCV does not share rec eptor specificity with the related polyomavirus, SV40.