The Journal of Experimental Medicine
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Published online 17 July 2000.
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© The Rockefeller University Press, 0022-1007/2000/7/289/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 2, July 17, 2000 289-294

Brief Definitive Report

Inhibition of Hepatitis B Virus Replication during Schistosoma mansoni Infection in Transgenic Mice

Heike McClarya, Rick Kocha, Francis V. Chisaria, and Luca G. Guidottia

a Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037
The Scripps Research Institute, Dept. of Molecular and Experimental Medicine, 10550 North Torrey Pines Rd., La Jolla, CA 92037.858-784-2960858-784-2758

guidotti{at}scripps.edu

Although coinfection of hepatitis B virus (HBV) and Schistosoma mansoni is a frequent event in humans, little is known about the interactions between these two pathogens. S. mansoni infection induces T helper cell type 2 (Th2)–type cytokines in the liver of humans and mice. The intrahepatic induction of nitric oxide (NO) and Th1-type cytokines, such as interferon (IFN)-{gamma} and IFN-{alpha}/β, inhibits HBV replication noncytopathically in the liver of transgenic mice. To examine whether S. mansoni infection and the accompanying induction of Th2-type cytokines could interfere with HBV replication in the liver, HBV transgenic mice were infected with S. mansoni. By 5 wk after infection, HBV replication disappeared concomitant with the intrahepatic induction of NO and Th1-type cytokines, and in the absence of Th2-type cytokines. By 6–8 wk after infection, HBV replication remained undetectable and this was associated with further induction of NO and Th1-type cytokines together with the appearance of Th2-type cytokines. The S. mansoni–dependent antiviral effect was partially blocked by genetically deleting IFN-{gamma}, although it was unaffected by deletion of IFN-{alpha}/β. These results indicate that IFN-{gamma} (probably via NO) mediates most of this antiviral activity and that Th2-type cytokines do not counteract the antiviral effect of IFN-{gamma}. Similar events may suppress HBV replication during human S. mansoni infection.

Key Words: transgenic/knockout • infectious immunity virus • helminth parasites • Th1/Th2 cytokines • liver

© 2000 The Rockefeller University Press


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