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Journal of Virology, August 2009, p. 7629-7640, Vol. 83, No. 15
0022-538X/09/$08.00+0     doi:10.1128/JVI.00679-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Baculovirus Induces Type I Interferon Production through Toll-Like Receptor-Dependent and -Independent Pathways in a Cell-Type-Specific Manner{triangledown}

Takayuki Abe,1 Yuuki Kaname,1 Xiaoyu Wen,1 Hideki Tani,1 Kohji Moriishi,1 Satoshi Uematsu,2 Osamu Takeuchi,2 Ken J. Ishii,2 Taro Kawai,2 Shizuo Akira,2 and Yoshiharu Matsuura1*

Department of Molecular Virology, Research Institute for Microbial Diseases,1 Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, Osaka, Japan2

Received 2 April 2009/ Accepted 19 May 2009

Autographa californica nuclear polyhedrosis virus (AcNPV) is a double-stranded-DNA virus that is pathogenic to insects. AcNPV was shown to induce an innate immune response in mammalian immune cells and to confer protection of mice from lethal viral infection. In this study, we have shown that production of type I interferon (IFN) by AcNPV in murine plasmacytoid dendritic cells (pDCs) and non-pDCs, such as peritoneal macrophages and splenic CD11c+ DCs, was mediated by Toll-like receptor (TLR)-dependent and -independent pathways, respectively. IFN regulatory factor 7 (IRF7) was shown to play a crucial role in the production of type I IFN by AcNPV not only in immune cells in vitro but also in vivo. In mouse embryonic fibroblasts (MEFs), AcNPV produced IFN-β and IFN-inducible chemokines through TLR-independent and IRF3-dependent pathways, in contrast to the TLR-dependent and IRF3/IRF7-independent production of proinflammatory cytokines. Although production of IFN-β and IFN-inducible chemokines was severely impaired in IFN promoter-stimulator 1 (IPS-1)-deficient MEFs upon infection with vesicular stomatitis virus, AcNPV produced substantial amounts of the cytokines in IPS-1-deficient MEFs. These results suggest that a novel signaling pathway(s) other than TLR- and IPS-1-dependent pathways participates in the production of type I IFN in response to AcNPV infection.

* Corresponding author. Mailing address: Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan. Phone: 81-6-6879-8340. Fax: 81-6-6879-8269. E-mail: matsuura{at}biken.osaka-u.ac.jp

{triangledown} Published ahead of print on 27 May 2009.

Journal of Virology, August 2009, p. 7629-7640, Vol. 83, No. 15
0022-538X/09/$08.00+0     doi:10.1128/JVI.00679-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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