The Journal of Experimental Medicine
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Published online 21 August 2000.
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© The Rockefeller University Press, 0022-1007/2000/8/529/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 4, August 21, 2000 529-536

Original Article

Host–Virus Interactions during Malaria Infection in Hepatitis B Virus Transgenic Mice

Valerie Pasquettoa, Luca G. Guidottia, Kazuhiro Kakimia, Moriya Tsujib, and Francis V. Chisaria
a Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037
b Department of Medical and Molecular Parasitology, New York University, School of Medicine, New York, New York 10010

Correspondence to: Francis V. Chisari, Department of Molecular and Experimental Medicine, Division of Experimental Pathology, The Scripps Research Institute, 10550 North Torrey Pines Rd., La Jolla, CA 92037. Tel:858-784-8228 Fax:858-784-2160 E-mail:fchisari{at}scripps.edu.

We have previously shown that hepatitis B virus (HBV) replication is abolished in the liver of HBV transgenic mice by inflammatory cytokines induced by HBV-specific cytotoxic T cells and during unrelated viral infections of the liver. We now report that intrahepatic HBV replication is also inhibited in mice infected by the malaria species Plasmodium yoelii 17X NL. P. yoelii infection triggers an intrahepatic inflammatory response characterized by the influx of natural killer cells, macrophages, and T cells. During this process, interferon (IFN)-{gamma} and IFN-{alpha}/ß suppress HBV gene expression and replication in the liver. Collectively, the data suggest that malaria infection might influence the course and pathogenesis of HBV infection in coinfected humans.

Key Words: hepatitis B virus transgenic mice, Plasmodium yoelii, inflammatory cells, inflammatory cytokines, liver


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