Cocaine potentiates the switch between latency and replication of Epstein-Barr virus in Raji cells.
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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ABSTRACT: The high prevalence of contaminated cell cultures suggests that viral contaminations might be distributed among cultures. We investigated more than 460 primate cell lines for Epstein-Barr (EBV), hepatitis B (HBV), hepatitis C (HCV), human immunodeficiency virus type 1 (HIV-1), human T-cell leukemia/lymphoma virus I and II (HTLV-I/-II), and squirrel monkey retrovirus (SMRV) infections for risk assessment. None of the cell lines were infected with HCV, HIV-1, or HTLV-I/-II. However, one cell line displayed reverse transcriptase activity. Thirty-nine cell lines harbored EBV DNA sequences. Studies on the lytic phase of EBV revealed that five cell lines produce EBV particles and six further cell lines produced EBV upon stimulation. One cell line contained an integrated HBV genome fragment but showed no virus production. Six cell lines were SMRV-infected. Newly established cell lines should be tested for EBV infections to detect B-lymphoblastoid cell lines (B-LCL). B-LCLs established with EBV from cell line B95-8 should be tested for SMRV infections.BioMed Research International 01/2010; 2010:904767. · 2.88 Impact Factor
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ABSTRACT: The strong inverse association between maternal age and risk of gastroschisis in offspring has spurred many investigators to hypothesize that behaviors among younger females are the cause. Examples include cigarette smoking, illicit drugs, genitourinary infections, and sexually transmitted diseases, each of which has been reported to be associated with gastroschisis. Although these exposures are more common in young women, recent studies have shown that cigarette smoking, genitourinary infections, and sexually transmitted diseases are most strongly associated with gastroschisis in older women. There is both anecdotal and published evidence showing that gastroschisis sometimes (but not always) occurs in clusters, raising the possibility that an infectious agent might be involved in its pathogenesis. One such agent whose epidemiologic characteristics parallel those of gastroschisis is Epstein-Barr virus (EBV). Primary EBV infection in early childhood has been decreasing over time, leaving a greater proportion of adolescents at risk, as reflected by increased rates of infectious mononucleosis over time. During the childbearing years, risk of primary EBV infection decreases dramatically, as does risk of gastroschisis. The stronger risks of gastroschisis associated with cigarette smoking, genitourinary infections, and sexually transmitted diseases in older women might be explained by EBV reactivation resulting from multiple challenges to immune response such as pregnancy, age, toxic exposures, and genitourinary and sexually transmitted infections. EBV and other herpes viruses should be added to the research agenda for gastroschisis.Birth Defects Research Part A Clinical and Molecular Teratology 11/2009; 88(2):71-5. · 2.27 Impact Factor
- Biomedecine [?] Pharmacotherapy 10/2001; 55(7):343-7. · 2.07 Impact Factor