Host-virus interactions during malaria infection in hepatitis B virus transgenic mice

We have previously shown that hepatitis B virus (HBV) replication is abolis hed in the liver of HBV transgenic mice by inflammatory cytokines induced b y HBV-specific cytotoxic T cells and during unrelated viral infections of t he liver. We now report that intrahepatic HBV replication is also inhibited in mice infected by the malaria species Plasmodium yoelii 17X NL. P. yoeli i 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/beta suppress HBV gene expres sion and replication in the liver. Collectively, the data suggest that mala ria infection might influence the course and pathogenesis of HBV infection in coinfected humans.