Molecular basis for resistance of herpes simplex virus type 1 mutants to the sulfated oligosaccharide inhibitor PI-88

Virology. 2007 Oct 25;367(2):244-52. doi: 10.1016/j.virol.2007.05.040. Epub 2007 Jul 2.

Abstract

Herpes simplex virus type 1 variants selected by virus propagation in cultured cells in the presence of the sulfated oligosaccharide PI-88 were analyzed. Many of these variants were substantially resistant to the presence of PI-88 during their initial infection of cells and/or their cell-to-cell spread. Nucleotide sequence analysis revealed that the deletion of amino acids 33-116 of gC but not lack of gC expression provided the virus with selective advantage to infect cells in the presence of PI-88. Purified gC (Delta33-116) was more resistant to PI-88 than unaltered protein in its binding to cells. Alterations that partly contributed to the virus resistance to PI-88 in its cell-to-cell spread activity were amino acid substitutions Q27R in gD and R770W in gB. These results suggest that PI-88 targets several distinct viral glycoproteins during the course of initial virus infection and cell-to-cell spread.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Amino Acids / metabolism
  • Animals
  • DNA, Viral
  • Drug Resistance, Microbial / genetics*
  • Herpesvirus 1, Human / drug effects*
  • Herpesvirus 1, Human / genetics*
  • Herpesvirus 1, Human / metabolism
  • Humans
  • Mutation
  • Oligosaccharides / pharmacology*
  • Tumor Cells, Cultured
  • Viral Envelope Proteins / drug effects*
  • Viral Envelope Proteins / genetics

Substances

  • Amino Acids
  • DNA, Viral
  • Oligosaccharides
  • Viral Envelope Proteins
  • glycoprotein gC, herpes simplex virus type 1
  • phosphomannopentaose sulfate