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

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...

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Autores principales: Pasquetto, Valerie, Guidotti, Luca G., Kakimi, Kazuhiro, Tsuji, Moriya, Chisari, Francis V.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2000
Materias:
Original Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193244/
https://www.ncbi.nlm.nih.gov/pubmed/10952722
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author Pasquetto, Valerie
Guidotti, Luca G.
Kakimi, Kazuhiro
Tsuji, Moriya
Chisari, Francis V.
author_facet Pasquetto, Valerie
Guidotti, Luca G.
Kakimi, Kazuhiro
Tsuji, Moriya
Chisari, Francis V.
author_sort Pasquetto, Valerie
collection PubMed
description 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.
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spelling pubmed-21932442008-04-16 Host–Virus Interactions during Malaria Infection in Hepatitis B Virus Transgenic Mice Pasquetto, Valerie Guidotti, Luca G. Kakimi, Kazuhiro Tsuji, Moriya Chisari, Francis V. J Exp Med Original Article 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. The Rockefeller University Press 2000-08-21 /pmc/articles/PMC2193244/ /pubmed/10952722 Text en © 2000 The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Original Article
Pasquetto, Valerie
Guidotti, Luca G.
Kakimi, Kazuhiro
Tsuji, Moriya
Chisari, Francis V.
Host–Virus Interactions during Malaria Infection in Hepatitis B Virus Transgenic Mice
title Host–Virus Interactions during Malaria Infection in Hepatitis B Virus Transgenic Mice
title_full Host–Virus Interactions during Malaria Infection in Hepatitis B Virus Transgenic Mice
title_fullStr Host–Virus Interactions during Malaria Infection in Hepatitis B Virus Transgenic Mice
title_full_unstemmed Host–Virus Interactions during Malaria Infection in Hepatitis B Virus Transgenic Mice
title_short Host–Virus Interactions during Malaria Infection in Hepatitis B Virus Transgenic Mice
title_sort host–virus interactions during malaria infection in hepatitis b virus transgenic mice
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193244/
https://www.ncbi.nlm.nih.gov/pubmed/10952722
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