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

Valerie Pasquetto, Luca G. Guidotti, Kazuhiro Kakimi, Moriya Tsuji, Francis V. Chisari

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)529-535
Number of pages7
JournalJournal of Experimental Medicine
Issue number4
Publication statusPublished - Aug 21 2000


  • Hepatitis B virus transgenic mice
  • Inflammatory cells
  • Inflammatory cytokines
  • Liver
  • Plasmodium yoelii

ASJC Scopus subject areas

  • Immunology


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