Echovirus infection of rhabdomyosarcoma cells is inhibited by antiserum to the complement control protein CD59

IG Goodfellow, RM Powell, T Ward, OB Spiller, JW Almond, DJ Evans*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)

Abstract

A number of echoviruses use decay accelerating factor (DAF) as a cellular receptor 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 coefficient ('A' particles) which are considered indicative of the particle uncoating process. We have previously demonstrated that antibodies to beta(2)-microglobulin 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 surface. We demonstrate here that antiserum to CD59 specifically blocks infection 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.

Original languageEnglish
Pages (from-to)1393-1401
Number of pages9
JournalJournal of General Virology
Volume81
Publication statusPublished - May 2000

Keywords

  • DECAY-ACCELERATING FACTOR
  • GPI-ANCHORED PROTEINS
  • REGULATORY PROTEIN
  • CELLULAR RECEPTOR
  • CROSS-LINKING
  • FACTOR DAF
  • POLIOVIRUS
  • MEMBRANES
  • CAVEOLAE
  • CLONING

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