There is evidence that CD46 (membrane cofactor protein) is a cellular
receptor for vaccine and laboratory-passaged strains of measles virus
(MV). Following infection with these MV strains, CD46 is downregulated
from the cell surface, and consequent complement-mediated lysis has b
een shown to occur upon infection of a human monocytic cell line. The
MV hemagglutinin (H) protein alone is capable of inducing this downreg
ulation. Some wild-type strains of MV fail to downregulate CD46, despi
te infection being prevented by anti-CD46 antibodies. In this study we
show that CD46 is also downregulated to the same extent by wild-type,
vaccine, and laboratory-passaged strains of rinderpest virus (RPV), a
lthough CD46 did not appear to be the receptor for RPV. Expression of
the RPV H protein by a nonreplicating adenovirus vector was also found
to cause this downregulation. A vaccine strain of peste des petits ru
minants virus caused slight downregulation of CD46 in infected Vero ce
lls, while wild-type and vaccine strains of canine distemper virus and
a wild-type strain of dolphin morbillivirus failed to downregulate CD
46. Downregulation of CD46 can, therefore, be a function independent o
f the use of this protein as a virus receptor.