Article

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

Department of Experimental Medicine and Biochemical Sciences, Microbiology, University of Rome Tor Vergata, Rome, Italy.
Biochemical and Biophysical Research Communications (Impact Factor: 2.28). 11/1999; 264(1):33-6. DOI: 10.1006/bbrc.1999.1447
Source: PubMed

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.

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