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Journal of Virology, August 2007, p. 8016-8024, Vol. 81, No. 15
0022-538X/07/$08.00+0 doi:10.1128/JVI.00403-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Viral Immunology Laboratory, CHUL Research Center (CHUQ), and Université Laval, Québec, QC, Canada G1V-4G2,1 Centre for the Study of Host Resistance and Research Institute, McGill University Health Centre, and Departments of Medicine and Microbiology and Immunology, McGill University, Montréal, QC, Canada H3A 2B42
Received 25 February 2007/ Accepted 14 May 2007
Epstein-Barr virus (EBV) is a gammaherpesvirus infecting the majority of the human adult population in the world. TLR2, a member of the Toll-like receptor (TLR) family, has been implicated in the immune responses to different viruses including members of the herpesvirus family, such as human cytomegalovirus, herpes simplex virus type 1, and varicella-zoster virus. In this report, we demonstrate that infectious and UV-inactivated EBV virions lead to the activation of NF-
B through TLR2 using HEK293 cells cotransfected with TLR2-expressing vector along with NF-
B-Luc reporter plasmid. NF-
B activation in HEK293-TLR2 cells (HEK293 cells transfected with TLR2) by EBV was not enhanced by the presence of CD14. The effect of EBV was abrogated by pretreating HEK293-TLR2 cells with blocking anti-TLR2 antibodies or by preincubating viral particles with neutralizing anti-EBV antibodies 72A1. In addition, EBV infection of primary human monocytes induced the release of MCP-1 (monocyte chemotactic protein 1), and the use of small interfering RNA targeting TLR2 significantly reduced such a chemokine response to EBV. Taken together, these results indicate that TLR2 may be an important pattern recognition receptor in the immune response directed against EBV infection.
Published ahead of print on 23 May 2007.
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