Literature DB >> 15546128

Reactivation of Epstein-Barr virus from latency.

Wolfgang Amon1, Paul J Farrell.   

Abstract

The general problem in cancer treatment centres on finding agents that specifically affect cancer cells without damaging normal cells. The differences between cancer cells and normal cells are usually very subtle but about 15% of all human cancers involve a virus infection, for example the Epstein-Barr virus associated cancers. In these cancers, every tumour cell carries the virus in a latent infection but the number of normal cells infected is very low. So a treatment that could somehow cause the elimination of EBV infected cells would be very specific for the cancer in such cases. One potential approach could involve finding ways to reactivate the latent virus in cancer cells into the early part of the lytic cycle, impeding cell proliferation, targeting chemotherapeutic agents to the cancer and causing the cancer cells to become targets for immune surveillance. This review considers the mechanisms by which EBV reactivation is controlled and discusses possible therapeutic approaches. Copyright (c) 2004 John Wiley & Sons, Ltd.

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Year:  2005        PMID: 15546128     DOI: 10.1002/rmv.456

Source DB:  PubMed          Journal:  Rev Med Virol        ISSN: 1052-9276            Impact factor:   6.989


  76 in total

1.  Identification of a new class of small molecules that efficiently reactivate latent Epstein-Barr Virus.

Authors:  Nadezhda Tikhmyanova; David C Schultz; Theresa Lee; Joseph M Salvino; Paul M Lieberman
Journal:  ACS Chem Biol       Date:  2014-02-19       Impact factor: 5.100

2.  Soluble Epstein-Barr virus glycoproteins gH, gL, and gp42 form a 1:1:1 stable complex that acts like soluble gp42 in B-cell fusion but not in epithelial cell fusion.

Authors:  Austin N Kirschner; Jasmina Omerovic; Boris Popov; Richard Longnecker; Theodore S Jardetzky
Journal:  J Virol       Date:  2006-10       Impact factor: 5.103

3.  Multivalent sequence recognition by Epstein-Barr virus Zta requires cysteine 171 and an extension of the canonical B-ZIP domain.

Authors:  Pu Wang; Latasha Day; Paul M Lieberman
Journal:  J Virol       Date:  2006-09-13       Impact factor: 5.103

4.  Virus and cell RNAs expressed during Epstein-Barr virus replication.

Authors:  Jing Yuan; Ellen Cahir-McFarland; Bo Zhao; Elliott Kieff
Journal:  J Virol       Date:  2006-03       Impact factor: 5.103

5.  Topoisomerase I and RecQL1 function in Epstein-Barr virus lytic reactivation.

Authors:  Pu Wang; Andrew J Rennekamp; Yan Yuan; Paul M Lieberman
Journal:  J Virol       Date:  2009-06-03       Impact factor: 5.103

6.  Contribution of myocyte enhancer factor 2 family transcription factors to BZLF1 expression in Epstein-Barr virus reactivation from latency.

Authors:  Takayuki Murata; Yohei Narita; Atsuko Sugimoto; Daisuke Kawashima; Teru Kanda; Tatsuya Tsurumi
Journal:  J Virol       Date:  2013-07-10       Impact factor: 5.103

7.  Activation of human herpesvirus replication by apoptosis.

Authors:  Alka Prasad; Jill Remick; Steven L Zeichner
Journal:  J Virol       Date:  2013-07-24       Impact factor: 5.103

8.  Pheno- and genotypic features of Epstein-Barr virus associated B-cell lymphoproliferations in peripheral T-cell lymphomas.

Authors:  Gábor Smuk; Arpád Illés; Katalin Keresztes; László Kereskai; Balázs Márton; Zsófia Nagy; Agnes Lacza; László Pajor
Journal:  Pathol Oncol Res       Date:  2009-12-17       Impact factor: 3.201

9.  Activation and repression of Epstein-Barr Virus and Kaposi's sarcoma-associated herpesvirus lytic cycles by short- and medium-chain fatty acids.

Authors:  Kelly L Gorres; Derek Daigle; Sudharshan Mohanram; George Miller
Journal:  J Virol       Date:  2014-05-07       Impact factor: 5.103

10.  Rhesus lymphocryptovirus type 1-associated B-cell nasal lymphoma in SIV-infected rhesus macaques.

Authors:  A K Marr-Belvin; A K Carville; M A Fahey; K Boisvert; S A Klumpp; M Ohashi; F Wang; S P O'Neil; S V Westmoreland
Journal:  Vet Pathol       Date:  2008-11       Impact factor: 2.221

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