Tromantadine inhibits a late step in herpes simplex virus type 1 replication and syncytium formation

Dawn E. Ickes, Tom M. Venetta, Yupa Phonphok, Ken S. Rosenthal

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

Addition of tromantadine after virus penetration inhibited HSV-1 induced syncytium formation and virus production in HEp-2 and VERO cells and acted additively with neutralizing antibody in blocking virus spread and cytopathology. Inhibition of syncytium formation in VERO cells infected with 0.01 pfu/cell of HSV-1 GC+ was observed at a concentration <25 μg/ml. The extent of inhibition was dependent upon the multiplicity of infection and cell type. Tromantadine inhibited a late event in HSV-1 replication which appeared to be sensitive to cycloheximide. Reversal of the inhibitory effect of tromantadine on syncytium formation required new protein synthesis. HSV-1 gB, gC, and gD were synthesized in the presence of tromantadine and could be detected on the cell surface by immunofluorescence. Tromantadine most likely inhibits a cellular process that is required for syncytium formation, such as glycoprotein processing, which occurs after the synthesis of the fusion protein but before its expression on the cell surface.

Original languageEnglish (US)
Pages (from-to)75-85
Number of pages11
JournalAntiviral Research
Volume14
Issue number2
DOIs
StatePublished - Aug 1990
Externally publishedYes

Keywords

  • Fusion
  • HSV-1
  • Syncytium formation
  • Tromantadine

ASJC Scopus subject areas

  • Pharmacology
  • Virology

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