HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Schaadt, E. Articles by Adler, B. Search for Related Content PubMed PubMed Citation Articles by Schaadt, E. Articles by Adler, B. Agricola Articles by Schaadt, E. Articles by Adler, B.

Epstein–Barr virus latent membrane protein 2A mimics B-cell receptor-dependent virus reactivation

Eveline Schaadt

Barbara Adler

GSF-Research Center for Environment and Health, Institute for Clinical Molecular Biology and Tumor Genetics, Marchioninistrasse 25, D-81377 Munich, Germany

Correspondence
Barbara Adler
adlerb{at}lmb.uni-muenchen.de

Latent membrane protein 2A (LMP2A) of Epstein–Barr virus (EBV) shares protein motifs with the B-cell receptor that play a role in B-cell receptor signalling and has been shown to mimic an activated B-cell receptor by providing a survival signal for mature B cells in transgenic mice. Conversely, LMP2A has been reported not to support but to inhibit B-cell receptor signalling with respect to virus reactivation and to block lytic virus induction after anti-Ig treatment of EBV-infected B cells. To solve this apparent paradox, the role of LMP2A in lytic-cycle induction was re-examined in B cells conditionally immortalized by EBV. It was shown that, in the absence of other stimuli, LMP2A expression alone could lead to induction of the virus lytic cycle. Similarly to B-cell receptor stimulation by anti-Ig treatment, this LMP2A-mediated reactivation was dependent on the mitogen-activated protein kinase pathway and could be inhibited by the viral LMP1. Our data reinforce the notion that LMP2A is a functional homologue of the B-cell receptor, not only with respect to B-cell survival but also with respect to regulation of the lytic cycle.

Present address: MorphoSys AG, Martinsried, Germany.

Present address: Max von Pettenkofer Institute, Genecenter, Feodor-Lynen-Strasse 25, D-81377 Munich, Germany.

This article has been cited by other articles:

				N. Agmon-Levin, M. Blank, Z. Paz, and Y. Shoenfeld Molecular mimicry in systemic lupus erythematosus Lupus, November 1, 2009; 18(13): 1181 - 1185. [Abstract] [PDF]

				M. P. Rechsteiner, C. Berger, L. Zauner, J. A. Sigrist, M. Weber, R. Longnecker, M. Bernasconi, and D. Nadal Latent Membrane Protein 2B Regulates Susceptibility to Induction of Lytic Epstein-Barr Virus Infection J. Virol., February 15, 2008; 82(4): 1739 - 1747. [Abstract] [Full Text] [PDF]

				C. Mancao and W. Hammerschmidt Epstein-Barr virus latent membrane protein 2A is a B-cell receptor mimic and essential for B-cell survival Blood, November 15, 2007; 110(10): 3715 - 3721. [Abstract] [Full Text] [PDF]

				M. Rovedo and R. Longnecker Epstein-Barr Virus Latent Membrane Protein 2B (LMP2B) Modulates LMP2A Activity J. Virol., January 1, 2007; 81(1): 84 - 94. [Abstract] [Full Text] [PDF]

				M. Swanson-Mungerson, R. Bultema, and R. Longnecker Epstein-Barr Virus LMP2A Enhances B-Cell Responses In Vivo and In Vitro J. Virol., July 15, 2006; 80(14): 6764 - 6770. [Abstract] [Full Text] [PDF]

				M. M. Brinkmann and T. F. Schulz Regulation of intracellular signalling by the terminal membrane proteins of members of the Gammaherpesvirinae. J. Gen. Virol., May 1, 2006; 87(Pt 5): 1047 - 1074. [Abstract] [Full Text] [PDF]