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Journal of Virology, June 2005, p. 7269-7272, Vol. 79, No. 11
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.11.7269-7272.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Toll-Like Receptor Signaling Inhibits Hepatitis B Virus Replication In Vivo{dagger}

Masanori Isogawa, Michael D. Robek, Yoshihiro Furuichi, and Francis V. Chisari*

Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037

Received 12 October 2004/ Accepted 24 January 2005

Toll-like receptors (TLR) play a key role in innate immunity. To examine the ability of diverse TLRs to modulate hepatitis B virus (HBV) replication, HBV transgenic mice received a single intravenous injection of ligands specific for TLR2, TLR3, TLR4, TLR5, TLR7, and TLR9. All of the ligands except for TLR2 inhibited HBV replication in the liver noncytopathically within 24 h in a {alpha}/ß interferon-dependent manner. The ability of these TLR ligands to induce antiviral cytokines at the site of HBV replication suggests that TLR activation could represent a powerful and novel therapeutic strategy for the treatment of chronic HBV infection.

* Corresponding author. Mailing address: The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037. Phone: (858) 784-8228. Fax: (858) 784-2160. E-mail: fchisari{at}scripps.edu.

{dagger} This is manuscript number 16835-MEM from The Scripps Research Institute.

Journal of Virology, June 2005, p. 7269-7272, Vol. 79, No. 11
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.11.7269-7272.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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