Virus entry is a major determinant of cell tropism of Edmonston and wild-type strains of measles virus as revealed by vesicular stomatitis virus pseudotypes bearing their envelope proteins

The Edmonston strain of measles virus (MV) that utilizes the human CD46 as the cellular receptor produced cytopathic effects (CPE) in all of the prima te cell lines examined. In contrast, the wild-type MV strains isolated in a marmoset B-cell line B95a (the KA and Ichinose strains) replicated and pro duced CPE in some but not all of the primate lymphoid cell lines. To determ ine the mechanism underlying this difference in cell tropism, we used a rec ently developed recombinant vesicular stomatitis virus (VSV) containing as a reporter the green fluorescent protein gene in lieu of the VSV G protein gene (VSV Delta G*). MV glycoproteins were efficiently incorporated into VS V Delta G*, producing the VSV pseudotypes. VSV Delta G* complemented with V SV G protein efficiently infected all of the cell lines tested. The VSV pse udotype bearing the Edmonston hemagglutinin (H) and fusion (F) protein (VSV Delta G*-EdHF) infected all cell lines in which the Edmonston strain cause d CPE, including the rodent cell lines to which the human CD46 gene was sta bly transfected. The pseudotype bearing the wild-type KA H protein and Edmo nston F protein (VSV Delta G*-KAHF) infected all lymphoid cell lines in whi ch the wild type MV strains caused CPE as efficiently as VSV Delta G*-EdHF, but it did not infect any of the cell lines resistant to infection with th e KA strain. The results indicate that the difference in cell tropism betwe en these MV strains was largely determined by virus entry, in which the H p roteins of respective MV strains play a decisive role.