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

Author:

Pasquetto Valerie1,Guidotti Luca G.1,Kakimi Kazuhiro1,Tsuji Moriya2,Chisari Francis V.1

Affiliation:

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

2. Department of Medical and Molecular Parasitology, New York University, School of Medicine, New York, New York 10010

Abstract

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)-γ and IFN-α/β 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.

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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