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Originally published In Press as doi:10.1074/jbc.M006671200 on February 5, 2001

J. Biol. Chem., Vol. 276, Issue 19, 16399-16405, May 11, 2001
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Hepatitis C Virus Core Protein Activates Nuclear Factor kappa B-dependent Signaling through Tumor Necrosis Factor Receptor-associated Factor*

Hideo Yoshida, Naoya KatoDagger , Yasushi Shiratori, Motoyuki Otsuka, Shin Maeda, Jun Kato, and Masao Omata

From the Department of Gastroenterology, Faculty of Medicine, University of Tokyo, Tokyo 113-8655, Japan

Hepatitis C virus (HCV) core protein, a viral nucleocapsid, has been shown to affect various intracellular events including the nuclear factor kappa B (NF-kappa B) signaling supposedly associated with inflammatory response, cell proliferation, and apoptosis. In order to elucidate the effect of HCV core protein on the NF-kappa B signaling in HeLa and HepG2 cells, a reporter assay was utilized. HCV core protein significantly activated NF-kappa B signaling in a dose-dependent manner not only in HeLa and HepG2 cells transiently transfected with core protein expression plasmid, but also in HeLa cells induced to express core protein under the control of doxycycline. HCV core protein increased the DNA binding affinity of NF-kappa B in the electrophoretic mobility shift assay. Acetyl salicylic acid, an IKKbeta -specific inhibitor, and dominant negative form of IKKbeta significantly blocked NF-kappa B activation by HCV core protein, suggesting HCV core protein activates the NF-kappa B pathway mainly through IKKbeta . Moreover, the dominant negative forms of TRAF2/6 significantly blocked activation of the pathway by HCV core protein, suggesting HCV core protein mimics proinflammatory cytokine activation of the NF-kappa B pathway through TRAF2/6. In fact, HCV core protein activated interleukin-1beta promoter mainly through NF-kappa B pathway. Therefore, this function of HCV core protein may play an important role in the inflammatory reaction induced by this hepatotropic virus.

* This work was supported in part by the Program for Promotion of Fundamental Studies in Health Sciences of the Organization for Pharmaceutical Safety and Research of Japan.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger To whom correspondence should be addressed. Tel.: 81-3-3815-5411 (ext. 33070); Fax: 81-3-3814-0021; E-mail: kato-2im@h.u-tokyo.ac.jp.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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