Ig. Goodfellow et al., Echovirus infection of rhabdomyosarcoma cells is inhibited by antiserum tothe complement control protein CD59, J GEN VIROL, 81, 2000, pp. 1393-1401
A number of echoviruses use decay accelerating factor (DAF) as a cellular r
eceptor or attachment protein for cell infection. Binding of echovirus 7 to
DAF at the cell surface, but not to soluble DAF in solution, triggers the
formation of virus particles exhibiting an altered sedimentation coefficien
t ('A' particles) which are considered indicative of the particle uncoating
process. We have previously demonstrated that antibodies to beta(2)-microg
lobulin block cell infection at a stage prior to 'A' particle formation and
suggested that this reflects the involvement of beta(2)-microglobulin (or
the associated MHC-I) in a virus-receptor complex that forms at the cell su
rface. We demonstrate here that antiserum to CD59 specifically blocks infec
tion of rhabdomyosarcoma cells by a range of echoviruses, including viruses
that bind DAF (e.g, echovirus 7) and those that use currently unidentified
receptors other than DAF. The block occurs prior to 'A' particle formation
and is cell-type specific. The potential role of CD59 as an active member,
or passive participant, in the virus-receptor complex is discussed.