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Silencing of latent membrane protein 2B reduces susceptibility to activation of lytic Epstein–Barr virus in Burkitt's lymphoma Akata cells

David Nadal

Michele Bernasconi

Experimental Infectious Diseases and Cancer Research, University Children's Hospital of Zurich, Zurich, Switzerland

Correspondence
David Nadal
david.nadal{at}kispi.unizh.ch
Michele Bernasconi
michele.bernasconi{at}kispi.unizh.ch

Epstein–Barr virus (EBV) latent membrane protein 2A (LMP2A) blocks B-cell receptor (BCR) signalling after BCR cross-linking to inhibit activation of lytic EBV, and ectopically expressed LMP2B negatively regulates LMP2A. Here, it is demonstrated that silencing of LMP2B in EBV-harbouring Burkitt's lymphoma Akata cells results in reduced expression of EBV immediate-early lytic BZLF1 gene mRNA and late lytic gp350/220 protein upon BCR cross-linking. Similarly, reduction of lytic EBV activation was observed in Akata cells overexpressing LMP2A. In contrast, silencing of LMP2A expression resulted in higher lytic EBV mRNA and protein expression in BCR cross-linked Akata cells. These observations indicate a role for LMP2B distinct from that of LMP2A in regulation of lytic EBV activation in the host cell and support the hypothesis that LMP2B exhibits a negative-regulatory effect on the ability of LMP2A to maintain EBV latency by preventing the switch to lytic replication.

These authors contributed equally to this work.

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				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]