Inhibition of HSV-1 multiplication in rat embryo fibroblasts constitutively expressing the EJ-ras oncogene

Virology. 1990 Nov;179(1):208-16. doi: 10.1016/0042-6822(90)90290-8.

Abstract

In order to examine cellular gene involvement in HSV-1 expression, we constructed different rat embryo fibroblast cell lines immortalized by adenovirus E1A or c-myc, with or without the human EJ bladder carcinoma transforming oncogene EJ-ras. HSV-1 multiplication was strongly inhibited in cells expressing EJ-ras genes compared to immortalized control cells. Virus adsorption and penetration were not quantitatively modified, but HSV-1 DNA replication was inhibited. The expression of viral thymidine kinase (TK) activity after infection by recombinant virus with the TK coding sequence under immediate-early (IE) promoter control showed that IE gene expression is inhibited in cells expressing EJ-ras. Analysis of IE gene transcription by Northern-blot hybridization and by nuclear run-off transcription assay indicates that this inhibition takes place at the transcriptional level.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenovirus Early Proteins
  • Adenoviruses, Human / genetics
  • Animals
  • Cell Nucleus / metabolism
  • Cell Transformation, Neoplastic*
  • Cells, Cultured
  • DNA Replication*
  • Embryo, Mammalian
  • Fibroblasts / cytology
  • Fibroblasts / enzymology
  • Genes, Viral
  • Genes, ras*
  • Humans
  • Nucleic Acid Hybridization
  • Oncogene Proteins, Viral / genetics
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Rats
  • Rats, Inbred F344
  • Restriction Mapping
  • Simplexvirus / physiology*
  • Thymidine Kinase / metabolism
  • Transcription, Genetic
  • Transfection
  • Vero Cells
  • Virus Replication*

Substances

  • Adenovirus Early Proteins
  • Oncogene Proteins, Viral
  • RNA, Messenger
  • Thymidine Kinase