Butyrate-induced reversal of herpes simplex virus restriction in neuroblastoma cells

Virology. 1986 Dec;155(2):584-92. doi: 10.1016/0042-6822(86)90218-7.


The synthesis of herpes simplex virus (HSV) in mouse neuroblastoma cells (NB, clone 41A3) is restricted. There was a disappearance of infectious virus upon serial passage of infected cells. NB cells treated with sodium-n-butyrate for 24 hr before infection synthesized 200-2000 times more HSV than untreated cells. Infectious center assays demonstrated that the number of cells capable of producing HSV was increased as a result of butyrate pretreatment. Although host protein synthesis was inhibited by HSV infection, viral-induced protein and DNA syntheses were not detected in the absence of butyrate. Cycloheximide blocked the induction of permissiveness by butyrate suggesting that a protein(s) was responsible for allowing HSV synthesis in NB cells. Regulatable host factors involved in HSV replication in neural cells can be studied in the system described.

MeSH terms

  • Animals
  • Bucladesine / pharmacology
  • Butyrates / pharmacology*
  • Butyric Acid
  • Cell Division / drug effects
  • Cell Line
  • DNA, Viral / biosynthesis
  • Fatty Acids / pharmacology
  • Mice
  • Neuroblastoma / microbiology*
  • Nucleic Acids / biosynthesis
  • Protein Biosynthesis
  • Simplexvirus / growth & development*
  • Structure-Activity Relationship
  • Time Factors
  • Virus Replication / drug effects*


  • Butyrates
  • DNA, Viral
  • Fatty Acids
  • Nucleic Acids
  • Butyric Acid
  • Bucladesine