A SINGLE AMINO-ACID CHANGE IN THE HEMAGGLUTININ PROTEIN OF MEASLES-VIRUS DETERMINES ITS ABILITY TO BIND CD46 AND REVEALS ANOTHER RECEPTOR ON MARMOSET B-CELLS

This paper provides evidence for a measles virus receptor other than C D46 on transformed marmoset and human B cells. We first showed that mo st tissues of marmosets are missing the SCR1 domain of CD46, which is essential for the binding of Edmonston measles virus, a laboratory str ain that has been propagated in Vero monkey kidney cells. In spite of this deletion, the common marmoset was shown to be susceptible to infe ctions by wild-type isolates of measles virus, although they did not s upport Edmonston measles virus production. As one would expect from th ese results, measles virus could not be propagated in owl monkey or ma rmoset kidney cell lines, but surprisingly, both a wild-type isolate ( Montefiore 89) and the Edmonston laboratory strain of measles virus gr ew efficiently in B95-8 marmoset B cells. In addition, antibodies dire cted against CD46 had no effect on wild-type infections of marmoset B cells and only partially inhibited the replication of the Edmonston la boratory strain in the same cells. A direct binding assay with insect cells expressing the hemagglutinin (H) proteins of either the Edmonsto n or Montefiore 89 measles virus strains was used to probe the recepto rs on these B cells. Insect cells expressing Edmonston H but not the w ild-type H bound to rodent cells with CD46 on their surface. On the ot her hand, both the Montefiore 89 H and Edmonston H proteins adhered to marmoset and human B cells. Most wild-type H proteins have asparagine residues at position 481 and can be converted to a CD46-binding pheno type by replacement of the residue with tyrosine. Similarly, the Edmon ston H protein did not bind CD46 when its Tyr481 was converted to aspa ragine. However, this mutation did not affect the ability of Edmonston H to bind marmoset and human B cells. The preceding results provide e vidence, through the use of a direct binding assay, that a second rece ptor for measles virus is present on primate B cells.