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Journal of Virology, January 2009, p. 1140-1146, Vol. 83, No. 2
0022-538X/09/$08.00+0     doi:10.1128/JVI.00602-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Epstein-Barr Virus LF2: an Antagonist to Type I Interferon{triangledown}

Liguo Wu,1,2 Even Fossum,4 Chul Hyun Joo,5 Kyung-Soo Inn,1,3 Young Chul Shin,1 Eric Johannsen,6 Lindsey M. Hutt-Fletcher,7 Juergen Hass,4 and Jae U. Jung1,3*

Department of Microbiology and Molecular Genetics, Tumor Virology Division, New England Primate Research Center, Harvard Medical School, One Pine Hill Drive, Southborough, Massachusetts 01772,1 Department of Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129,2 Department of Molecular Microbiology and Immunology, University of Southern California Keck Medical School, 1200 Zonal Avenue, Los Angeles, California 93300,3 Institut für Genetik, Forschungszentrum Karlsruhe, Postfach 3640, Karlsruhe D-76021, Germany,4 Department of Microbiology, University of Ulsan College of Medicine, Seoul, South Korea 138-736,5 Department of Medicine, Channing Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115,6 Department of Microbiology and Immunology, Center for Molecular and Tumor Virology and Feist-Weiller Cancer Center, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, Louisiana 711307

Received 18 March 2008/ Accepted 26 September 2008

Upon viral infection, the major defense mounted by the host immune system is activation of the interferon (IFN)-mediated antiviral pathway, which is mediated by IFN regulatory factors (IRFs). In order to complete their life cycle, viruses must modulate host IFN-mediated immune responses. Despite its association with significant human health problems, activities of Epstein-Barr virus (EBV), a human tumor-inducing herpesvirus, to evade host IFN-mediated innate immunity have not been well characterized. To search for EBV genes that block IFN signal transduction, we carried out a screening of EBV open reading frames for their abilities to block IFN-{alpha}/β-mediated luciferase expression upon Sendai virus infection. This screening demonstrates that EBV LF2 tegument protein specifically interacts with the central inhibitory association domain of IRF7, and this interaction leads to inhibition of the dimerization of IRF7, which suppresses IFN-{alpha} production and IFN-mediated immunity. This demonstrates a novel immune evasion mechanism of EBV LF2 in blocking cellular IRF7-mediated innate immunity.

* Corresponding author. Mailing address: Molecular Microbiology & Immunology Department, University of Southern California, Keck School of Medicine, 2011 Zonal Avenue, HMR Rm. 401, Los Angeles, CA 90033. Phone: (323) 442-1713. Fax: (323) 442-1721. E-mail: jaeujung{at}usc.edu

{triangledown} Published ahead of print on 5 November 2008.

Journal of Virology, January 2009, p. 1140-1146, Vol. 83, No. 2
0022-538X/09/$08.00+0     doi:10.1128/JVI.00602-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Wang, J.-T., Doong, S.-L., Teng, S.-C., Lee, C.-P., Tsai, C.-H., Chen, M.-R. (2009). Epstein-Barr Virus BGLF4 Kinase Suppresses the Interferon Regulatory Factor 3 Signaling Pathway. J. Virol. 83: 1856-1869 [Abstract] [Full Text]  


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