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 Previous Article

Journal of Virology, January 2004, p. 544-549, Vol. 78, No. 1
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.1.544-549.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Epstein-Barr Virus Immediate-Early Protein BZLF1 Inhibits Tumor Necrosis Factor Alpha-Induced Signaling and Apoptosis by Downregulating Tumor Necrosis Factor Receptor 1

Thomas E. Morrison,1,2 Amy Mauser,2 Aloysius Klingelhutz,3 and Shannon C. Kenney1,2,4*

Department of Microbiology and Immunology,1 Department of Medicine,4 Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599,2 Department of Microbiology, University of Iowa, Iowa City, Iowa 522423

Received 11 July 2003/ Accepted 18 September 2003

Tumor necrosis factor alpha (TNF-{alpha}) is a key mediator of host immune and inflammatory responses and inhibits herpesvirus replication by cytolytic and noncytolytic mechanisms. TNF-{alpha} effects are primarily mediated through the major TNF-{alpha} receptor, TNF-R1, which is constitutively expressed in most cell types. Here we show that the Epstein-Barr virus (EBV) immediate-early protein BZLF1 prevents TNF-{alpha} activation of target genes and TNF-{alpha}-induced cell death. These effects are mediated by down-regulation of the promoter for TNF-R1. Additionally, we demonstrate that expression of TNF-R1 is downregulated during the EBV lytic replication cycle. Thus, EBV has developed a novel mechanism for evading TNF-{alpha} antiviral effects during lytic reactivation or primary infection.

* Corresponding author. Mailing address: Room 22-038, Lineberger Comprehensive Cancer Center, 102 Mason Farm Rd., CB #7295, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599. Phone: (919) 966-1248. Fax: (919) 966-8212. E-mail: shann{at}med.unc.edu.

Journal of Virology, January 2004, p. 544-549, Vol. 78, No. 1
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.1.544-549.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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