Cocaine potentiates the switch between latency and replication of Epstein-Barr virus in Raji cells

Biochem Biophys Res Commun. 1999 Oct 14;264(1):33-6. doi: 10.1006/bbrc.1999.1447.

Abstract

This paper shows that cocaine amplifies Epstein-Barr virus (EBV) reactivation in Raji cells. Its effect on early viral protein synthesis was maximal when it was added with 12-O-tetradecanoyl phorbol-13-acetate (TPA) plus n-butyrate, but nil when added alone. The enhancing effect of cocaine on early replicative stages of latent EBV was associated with an increase of Ca(2+) mobilization induced by the drug and with an induction of cellular protein phosphorylation in chemicals and cocaine-treated Raji cells. Cocaine also acted synergistically with TPA and n-butyrate to induce Z Epstein-Barr replication activator (ZEBRA), a nuclear phosphoprotein responsible for the activation of early viral gene expression. These findings provide the first evidence that cocaine may represent an important co-factor in the reactivation of early stages of latent EBV infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biological Transport / drug effects
  • Butyrates / pharmacology
  • Calcium / metabolism
  • Carcinogens / pharmacology
  • Cocaine / pharmacology*
  • DNA-Binding Proteins / biosynthesis
  • Drug Synergism
  • Herpesvirus 4, Human / drug effects*
  • Herpesvirus 4, Human / physiology
  • Humans
  • Phosphorylation / drug effects
  • Tetradecanoylphorbol Acetate / pharmacology
  • Trans-Activators / biosynthesis
  • Tumor Cells, Cultured
  • Viral Proteins*
  • Virus Latency / drug effects*
  • Virus Replication / drug effects*

Substances

  • BZLF1 protein, Herpesvirus 4, Human
  • Butyrates
  • Carcinogens
  • DNA-Binding Proteins
  • Trans-Activators
  • Viral Proteins
  • Cocaine
  • Tetradecanoylphorbol Acetate
  • Calcium