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The fibroblast growth-factor receptor is not required for herpes-simplex virus type-1 infection

Academic Article
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Overview

authors

  • Mirda, D. P.
  • Navarro, D.
  • Paz, P.
  • Lee, Pauline
  • Pereira, L.
  • Williams, L. T.

publication date

  • January 1992

journal

  • Journal of Virology  Journal

abstract

  • The early events mediating herpes simplex virus type 1 (HSV-1) infection include virion attachment to cell surface heparan sulfates and subsequent penetration. Recent evidence has suggested that the high-affinity fibroblast growth factor (FGF) receptor mediates HSV-1 entry. This report presents three lines of experimental evidence showing that the high-affinity FGF receptor is not required for HSV-1 infection. First, rat L6 myoblasts lacking FGF receptors were as susceptible to HSV-1 infection as L6 cells genetically engineered to express the FGF receptor. Second, a soluble FGF receptor fragment that inhibited FGF binding and receptor activation did not inhibit HSV-1 infection. Finally, basic FGF (but not acidic FGF) inhibited HSV-1 infection in L6 cells lacking FGF receptors, presumably by blocking cell surface heparan sulfates also required for HSV-1 infection. These results show that the high-affinity FGF receptor is not required for HSV-1 infection but instead that specific low-affinity basic FGF binding sites are used for HSV-1 infection.

subject areas

  • Animals
  • Cell Line
  • Fibroblast Growth Factors
  • Fluorescent Antibody Technique
  • Rats
  • Receptors, Cell Surface
  • Receptors, Fibroblast Growth Factor
  • Simplexvirus
  • Solubility
  • Transfection
  • Vero Cells
  • Virus Replication
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Identity

PubMed Central ID

  • PMC238305

International Standard Serial Number (ISSN)

  • 0022-538X

PubMed ID

  • 1309254
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Additional Document Info

start page

  • 448

end page

  • 457

volume

  • 66

issue

  • 1

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