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JAC Advance Access originally published online on July 1, 2003
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Journal of Antimicrobial Chemotherapy (2003) 52, 152-154
© 2003 The British Society for Antimicrobial Chemotherapy


Leading Article

Identification of latent membrane protein 2A (LMP2A) specific targets for treatment and eradication of Epstein–Barr virus (EBV)-associated diseases

Michelle Swanson-Mungerson, Masato Ikeda, Lori Lev, Richard Longnecker* and Toni Portis

Department of Microbiology and Immunology, Northwestern University Medical School, Chicago, IL 60611, USA

Keywords: antivirals, Epstein–Barr virus, tyrosine kinases, microarray analysis

The first 150 words of the full text of this article appear below.


    Introduction
 
Epstein–Barr Virus (EBV) is a human herpesvirus that establishes a lifelong latent infection in B lymphocytes. EBV is associated with the development of several malignancies of lymphoid origin, including Burkitt’s lymphoma, Hodgkin’s disease, and lymphoproliferative disorders arising in immunocompromised patients.1 There are also diseases of epithelial origin associated with EBV infection, including nasopharyngeal carcinoma and oral hairy leucoplakia.1

In vitro, EBV can transform infected lymphocytes into continuously proliferating lymphoblasts. In fact, most functional studies of EBV proteins have been carried out using lymphoblastoid cell lines (LCLs) established in vitro.2,3 Expression of viral latency-associated transcripts in vivo appears to be tightly regulated. Whereas viral Epstein–Barr nuclear antigen 1 (EBNA1), EBV-encoded RNAs (EBERs), latent membrane protein 1 (LMP1) and LMP2A transcripts have been detected in tumour cells from patients with EBV-associated malignancies, LMP2A is one of the most consistently identified in vivo in B cells from healthy individuals harbouring a . . . [Full Text of this Article]


    LMP2A and B cell receptor (BCR) signalling
 

    DNA microarray analysis of LMP2A-expressing cells
 

    Functional inhibitors to study LMP2A signalling
 

    Summary and concluding statement
 

    Acknowledgements
 

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