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Conserved receptor-binding domains of Lake Victoria marburgvirus and Zaire ebolavirus bind a common receptor

  1. Author:
    Kuhn, J. H.
    Radoshitzky, S. R.
    Guth, A. C.
    Warfield, K. L.
    Li, W. H.
    Vincent, M. J.
    Towner, J. S.
    Nichol, S. T.
    Bavari, S.
    Choe, H.
    Aman, M. J.
    Farzan, M.
  2. Author Address

    Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Dept Microbiol & Mol Genet, Southborough, MA 01772 USA. Free Univ Berlin, Dept Biol, D-14195 Berlin, Germany. USA, Med Res Inst Infect Dis, Frederick, MD 21702 USA. Ctr Dis Control & Prevent, Natl Ctr Infect Dis, Special Pathogens Branch, Atlanta, GA 30332 USA. Harvard Univ, Sch Med, Childrens Hosp, Dept Pediat, Boston, MA 02115 USA.;Farzan, M, Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Dept Microbiol & Mol Genet, 1 Pine Hill Dr, Southborough, MA 01772 USA.;farzan@hms.harvard.edu
    1. Year: 2006
    2. Date: Jun
  1. Journal: Journal of Biological Chemistry
    1. 281
    2. 23
    3. Pages: 15951-15958
  2. Type of Article: Article
  3. ISSN: 0021-9258
  1. Abstract:

    The GP(1,2) envelope glycoproteins (GP) of filoviruses (marburg- and ebolaviruses) mediate cell-surface attachment, membrane fusion, and entry into permissive cells. Here we show that a 151-amino acid fragment of the Lake Victoria marburgvirus GP1 subunit bound filovirus-permissive cell lines more efficiently than full-length GP1. An homologous 148-amino acid fragment of the Zaire ebolavirus GP1 subunit similarly bound the same cell lines more efficiently than a series of longer GP1 truncation variants. Neither the marburgvirus GP1 fragment nor that of ebolavirus bound a nonpermissive lymphocyte cell line. Both fragments specifically inhibited replication of infectious Zaire ebolavirus, as well as entry of retroviruses pseudotyped with either Lake Victoria marburgvirus or Zaire ebolavirus GP(1,2). These studies identify the receptor-binding domains of both viruses, indicate that these viruses utilize a common receptor, and suggest that a single small molecule or vaccine can be developed to inhibit infection of all filoviruses.

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External Sources

  1. DOI: 10.1074/jbc.M601796200
  2. WOS: 000237996000046

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