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Blood, 15 February 2004, Vol. 103, No. 4, pp. 1433-1437. Prepublished online as a Blood First Edition Paper on October 16, 2003; DOI 10.1182/blood-2003-08-2674. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-08-2674v1 103/4/1433    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Krug, A. Articles by Colonna, M. Search for Related Content PubMed PubMed Citation Articles by Krug, A. Articles by Colonna, M. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Herpes simplex virus type 1 activates murine natural interferon-producing cells through toll-like receptor 9 Anne Krug, Gary D. Luker, Winfried Barchet, David A. Leib, Shizuo Akira, and Marco Colonna From the Department of Pathology and Immunology, the Molecular Imaging Center, Mallinckrodt Institute of Radiology, the Departments of Molecular Microbiology, and the Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St Louis, MO; and the Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Japan. Natural interferon-producing cells (IPCs) specialize in the production of high levels of type 1 interferons (IFNs) in response to encapsulated DNA and RNA viruses. Here we demonstrate that the secretion of type 1 IFN in response to herpes simplex virus type 1 (HSV-1) in vitro is mediated by the toll-like receptor 9 (TLR9)/MyD88 pathway. Moreover, IPCs produce interleukin-12 (IL-12) in response to HSV-1 in vitro, which is also dependent on TLR9/ MyD88 signaling. Remarkably, though TLR9/MyD88-deficiency abrogates IPC responses to HSV-1 in vitro, mice lacking either MyD88 or TLR9 are capable of controlling HSV-1 replication in vivo after local infection, demonstrating that TLR9- and MyD88-independent pathways in cells other than IPCs can effectively compensate for defective IPC responses to HSV-1. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: V. D. Menachery and D. A. Leib Control of Herpes Simplex Virus Replication Is Mediated through an Interferon Regulatory Factor 3-Dependent Pathway J. Virol., December 1, 2009; 83(23): 12399 - 12406. 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