Chromosomal integration of Epstein ‐ Barr virus genomes in nasopharyngeal carcinoma cells

Chang, Yao; Cheng, Sou-De; Tsai, Ching-Hwa

doi:10.1002/hed.10039

Cited by 31 publications

(14 citation statements)

References 27 publications

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“…The EBV lytic program results in inhibition of host cellular DNA replication and disruption of DNA repair, leading to accumulation of unrepaired DNA and consequent genomic instability 36. Cytogenetic studies have suggested that genomic instability may be a common feature in the development of NPC 37–40. As HHR pathway proteins appear to play an important role in lytic reactivation of EBV virus, we hypothesized that the genes coding proteins involved in lytic reactivation of virus may influence seropositivity rates.…”

Section: Discussionmentioning

confidence: 99%

Lipase Catalysis in Ionic Liquids and Supercritical Carbon Dioxide at 150 °C

Lozano

Diego

Carrié

et al. 2003

Biotechnology Progress

143

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Free and immobilized Candida antarctica lipase B dispersed in ionic liquids (1-ethyl-3-methylimidazolium bistriflimide and 1-buthyl-3-methylimidazolium bistriflimide) were used as catalyst for the continuous kinetic resolution of rac-1-phenylethanol in supercritical carbon dioxide at 120 and 150 degrees C and 10 MPa. Excellent activity, stability and enantioselectivity levels were recorded in continuous operation.

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Section: Discussionmentioning

confidence: 99%

Lipase Catalysis in Ionic Liquids and Supercritical Carbon Dioxide at 150 °C

Lozano

Diego

Carrié

et al. 2003

Biotechnology Progress

143

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“…Cells were lysed and digested by proteinase K as described previously and then subjected to the following PCR analysis (Chang et al, 2002). Conventional PCR detection of BamHI W fragments of the EBV genome was performed following our previous protocol (Chang et al, 2002). For quantification of EBV DNA, real-time PCR was used according to the manufacturer's instructions (Applied Biosystems).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of the Epstein–Barr virus lytic cycle by Zta-targeted RNA interference

Chang

Lee

et al. 2004

Journal of General Virology

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Epstein-Barr virus (EBV) reactivation into the lytic cycle plays certain roles in the development of EBV-associated diseases, so an effective strategy to block the viral lytic cycle may be of value to reduce the disease risk or to improve the clinical outcome. This study examined whether the EBV lytic cycle could be inhibited using RNA interference (RNAi) directed against the essential viral gene Zta. In cases of EBV reactivation triggered by chemicals or by exogenous Rta, Zta-targeted RNAi prevented the induction of Zta and its downstream genes and further blocked the lytic replication of viral genomes. This antiviral effect of RNAi was not likely to be mediated by activation of the interferon pathway, as phosphorylation of STAT1 was not induced. In addition, novel EBV-infected epithelial cells showing constitutive activation of the lytic cycle were cloned; such established lytic infection was also suppressed by Zta-targeted RNAi. These results indicate that RNAi can be used to inhibit the EBV lytic cycle effectively in vitro and could also be of potential use to develop anti-EBV treatments. INTRODUCTIONEpstein-Barr virus (EBV), a gammaherpesvirus associated with several human diseases, has two phases in its life cycle: latent and lytic stages . During EBV latency, only a few so-called latent genes are expressed, whereas an expression cascade of numerous lytic genes occurs following reactivation of the lytic cycle. In latency, the copy number of viral DNA is maintained at a relatively low level and no virion is produced but, in the EBV lytic cycle, there is amplification of viral genomes and production of virus particles Metzenberg, 1990).The majority of EBV infection in vivo is latent and it is this type of infection that is observed in peripheral B lymphocytes of healthy carriers and in most tumour cells of EBV-associated cancers such as nasopharyngeal carcinoma (NPC), Hodgkin's disease (HD) and endemic Burkitt's lymphoma . Intriguingly, several clues indicate that EBV reactivation into the lytic cycle may play a role in the pathogenesis of these malignancies. Elevated antibody titres against EBV lytic antigens and increased viral DNA load in serum/plasma, two parameters that represent EBV reactivation in vivo, correlate with advanced cancer stages, poor prognosis or tumour recurrence after therapy (de-Vathaire et al., 1988;Henle et al., 1969Henle et al., , 1977Henle & Henle, 1976;Lei et al., 2000;Levine et al., 1971;Lo, 2001). Serological studies further suggest that EBV reactivation may occur months or years before the clinical diagnosis of NPC, HD and endemic Burkitt's lymphoma, serving as a risk factor of cancer development (Chien et al., 2001;Geser et al., 1982;Mueller et al., 1989;Zeng et al., 1985). Another notable clue comes from in vitro studies, in which the EBV lytic cycle was activated by extracts of some foodstuffs or plants that were identified as dietary or environmental risk factors of NPC or endemic Burkitt's lymphoma (Bouvier et al., 1995; MacNeil et al., 2003;Shao et al., 1988).The aetiolo...

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“…H2B4 cell, a nasopharyngeal carcinoma cell clone harboring one copy of the EBV genome was used as a positive control (14). In our series, once the PBMC EBV viral load above 100 copies/g PBMC DNA was noted, we rechecked the viral load 2 weeks later.…”

Section: Quantification Of Ebv Dna Viral Load In Peripheral Blood Monmentioning

confidence: 99%

Timing of Epstein-Barr Virus Acquisition and the Course of Posttransplantation Lymphoproliferative Disorder in Children

et al. 2009

Transplantation

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Chromosomal integration of Epstein ‐ Barr virus genomes in nasopharyngeal carcinoma cells

Cited by 31 publications

References 27 publications

Lipase Catalysis in Ionic Liquids and Supercritical Carbon Dioxide at 150 °C

Lipase Catalysis in Ionic Liquids and Supercritical Carbon Dioxide at 150 °C

Inhibition of the Epstein–Barr virus lytic cycle by Zta-targeted RNA interference

Timing of Epstein-Barr Virus Acquisition and the Course of Posttransplantation Lymphoproliferative Disorder in Children

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