Herpes simplex virus triggers and then disarms a host antiviral response

J Virol. 2001 Jan;75(2):750-8. doi: 10.1128/JVI.75.2.750-758.2001.

Abstract

Virus infection induces an antiviral response that is predominantly associated with the synthesis and secretion of soluble interferon. Here, we report that herpes simplex virus type 1 virions induce an interferon-independent antiviral state in human embryonic lung cells that prevents plaquing of a variety of viruses. Microarray analysis of 19,000 human expressed sequence tags revealed induction of a limited set of host genes, the majority of which are also induced by interferon. Genes implicated in controlling the intracellular spread of virus and eliminating virally infected cells were among those induced. Induction of the cellular response occurred in the absence of de novo cellular protein synthesis and required viral penetration. In addition, this response was only seen when viral gene expression was inhibited, suggesting that a newly synthesized viral protein(s) may function as an inhibitor of this response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Expressed Sequence Tags
  • Gene Expression Regulation*
  • Herpes Simplex Virus Protein Vmw65 / genetics
  • Herpes Simplex Virus Protein Vmw65 / metabolism
  • Herpesvirus 1, Human / genetics
  • Herpesvirus 1, Human / immunology
  • Herpesvirus 1, Human / pathogenicity
  • Herpesvirus 1, Human / physiology*
  • Humans
  • Immediate-Early Proteins / genetics
  • Immediate-Early Proteins / metabolism
  • Interferons / pharmacology
  • Oligonucleotide Array Sequence Analysis / methods
  • Signal Transduction
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Transcriptional Activation
  • Tumor Cells, Cultured
  • Viral Plaque Assay
  • Viral Proteins*
  • Virion / immunology

Substances

  • Herpes Simplex Virus Protein Vmw65
  • ICP47 protein, Herpes simplex virus
  • Immediate-Early Proteins
  • Transcription Factors
  • Viral Proteins
  • Interferons