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 Reports

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

Correspondence to: Luca G. Guidotti, The Scripps Research Institute, Dept. of Molecular and Experimental Medicine, 10550 North Torrey Pines Rd., La Jolla, CA 92037. Tel:858-784-2758 Fax:858-784-2960 E-mail: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}/ß, 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}/ß. 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


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