Viral-Load-Dependent Effects of Liver Injury and Regeneration on Hepatitis B Virus Replication in Mice
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| Published in | Journal of Virology Vol. 86; no. 18; pp. 9599 - 9605 |
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| ISSN | 0022-538X 1098-5514 1098-5514 |
| DOI | 10.1128/JVI.01087-12 |
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Hepatitis B virus (HBV) is a hepatotropic virus that can cause severe liver diseases. By conducting studies using four different transgenic mouse lines that carry either the wild-type HBV genome or the HBV genome incapable of expressing the X gene, we found that liver injury and regeneration induced by a partial hepatectomy (PHx) could have different effects on HBV replication depending on the mouse lines. Further studies using hydrodynamic injection to introduce different amounts of the HBV genomic DNA into the mouse liver revealed that liver injury and regeneration induced by PHx enhanced HBV replication when viral load was low and suppressed HBV replication when viral load was high. These effects of liver injury and regeneration on HBV were independent of the HBV X protein and apparently due to alpha and beta interferons (IFN-α/β), as the effects could be abolished by the injection of anti-IFN-α/β antibodies. Further analysis indicated that PHx could induce the expression of hepatocyte nuclear factor 3 gamma (HNF3γ) when viral load was low and activate the signal transducer and activator of transcription 3 (Stat3) and suppress the expression of the suppressor of cytokine signaling 3 (SOCS3) irrespective of viral load. As both HNF3γ and Stat3 are required to activate the HBV enhancer I to stimulate HBV gene expression and replication, these results provided an explanation to the viral-load-dependent effect of liver injury and regeneration on HBV replication. Our studies thus revealed a novel interaction between HBV and its host and provided important information for understanding HBV replication and pathogenesis during liver injury.Hepatitis B virus (HBV) is a hepatotropic virus that can cause severe liver diseases. By conducting studies using four different transgenic mouse lines that carry either the wild-type HBV genome or the HBV genome incapable of expressing the X gene, we found that liver injury and regeneration induced by a partial hepatectomy (PHx) could have different effects on HBV replication depending on the mouse lines. Further studies using hydrodynamic injection to introduce different amounts of the HBV genomic DNA into the mouse liver revealed that liver injury and regeneration induced by PHx enhanced HBV replication when viral load was low and suppressed HBV replication when viral load was high. These effects of liver injury and regeneration on HBV were independent of the HBV X protein and apparently due to alpha and beta interferons (IFN-α/β), as the effects could be abolished by the injection of anti-IFN-α/β antibodies. Further analysis indicated that PHx could induce the expression of hepatocyte nuclear factor 3 gamma (HNF3γ) when viral load was low and activate the signal transducer and activator of transcription 3 (Stat3) and suppress the expression of the suppressor of cytokine signaling 3 (SOCS3) irrespective of viral load. As both HNF3γ and Stat3 are required to activate the HBV enhancer I to stimulate HBV gene expression and replication, these results provided an explanation to the viral-load-dependent effect of liver injury and regeneration on HBV replication. Our studies thus revealed a novel interaction between HBV and its host and provided important information for understanding HBV replication and pathogenesis during liver injury. Hepatitis B virus (HBV) is a hepatotropic virus that can cause severe liver diseases. By conducting studies using four different transgenic mouse lines that carry either the wild-type HBV genome or the HBV genome incapable of expressing the X gene, we found that liver injury and regeneration induced by a partial hepatectomy (PHx) could have different effects on HBV replication depending on the mouse lines. Further studies using hydrodynamic injection to introduce different amounts of the HBV genomic DNA into the mouse liver revealed that liver injury and regeneration induced by PHx enhanced HBV replication when viral load was low and suppressed HBV replication when viral load was high. These effects of liver injury and regeneration on HBV were independent of the HBV X protein and apparently due to alpha and beta interferons (IFN-α/β), as the effects could be abolished by the injection of anti-IFN-α/β antibodies. Further analysis indicated that PHx could induce the expression of hepatocyte nuclear factor 3 gamma (HNF3γ) when viral load was low and activate the signal transducer and activator of transcription 3 (Stat3) and suppress the expression of the suppressor of cytokine signaling 3 (SOCS3) irrespective of viral load. As both HNF3γ and Stat3 are required to activate the HBV enhancer I to stimulate HBV gene expression and replication, these results provided an explanation to the viral-load-dependent effect of liver injury and regeneration on HBV replication. Our studies thus revealed a novel interaction between HBV and its host and provided important information for understanding HBV replication and pathogenesis during liver injury. |
| Author | Cheng-fu Kuo Jing-hsiung James Ou Wen-ling Chen Yongjun Tian |
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| Cites_doi | 10.1084/jem.20070820 10.1371/journal.ppat.1002159 10.1128/JVI.77.14.7707-7712.2003 10.1128/jvi.76.5.2579-2584.2002 10.1080/08941930390194424 10.1126/science.276.5309.60 10.1172/JCI11867 10.1128/jvi.71.6.4804-4808.1997 10.1007/s00534-010-0304-2 10.1073/pnas.202398599 10.1016/j.semcdb.2008.08.010 10.1002/hep.20969 10.1073/pnas.0911373107 10.1053/gast.1996.v110.pm8964411 10.1371/journal.ppat.1000986 10.1128/jvi.69.10.6158-6169.1995 10.1006/cyto.2000.0797 10.1016/j.jss.2005.12.011 10.1111/j.1440-1746.2010.06539.x 10.1038/cr.2010.183 |
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| Keywords | Virus Regeneration Vertebrata Mammalia Mouse Hepadnaviridae Liver Rodentia Orthohepadnavirus Replication Hepatitis B virus Viral load |
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| References_xml | – ident: e_1_3_2_13_2 doi: 10.1084/jem.20070820 – start-page: 2977 volume-title: Fields virology year: 2007 ident: e_1_3_2_16_2 – ident: e_1_3_2_18_2 doi: 10.1371/journal.ppat.1002159 – ident: e_1_3_2_23_2 doi: 10.1128/JVI.77.14.7707-7712.2003 – ident: e_1_3_2_21_2 doi: 10.1128/jvi.76.5.2579-2584.2002 – ident: e_1_3_2_6_2 doi: 10.1080/08941930390194424 – ident: e_1_3_2_11_2 doi: 10.1126/science.276.5309.60 – ident: e_1_3_2_3_2 doi: 10.1172/JCI11867 – ident: e_1_3_2_7_2 doi: 10.1128/jvi.71.6.4804-4808.1997 – ident: e_1_3_2_5_2 doi: 10.1007/s00534-010-0304-2 – ident: e_1_3_2_22_2 doi: 10.1073/pnas.202398599 – ident: e_1_3_2_15_2 doi: 10.1016/j.semcdb.2008.08.010 – ident: e_1_3_2_4_2 doi: 10.1002/hep.20969 – volume: 263 start-page: G579 year: 1992 ident: e_1_3_2_2_2 article-title: Antibodies to tumor necrosis factor-alpha inhibit liver regeneration after partial hepatectomy publication-title: Am. J. Physiol. – ident: e_1_3_2_17_2 doi: 10.1073/pnas.0911373107 – ident: e_1_3_2_19_2 doi: 10.1053/gast.1996.v110.pm8964411 – ident: e_1_3_2_20_2 doi: 10.1371/journal.ppat.1000986 – ident: e_1_3_2_8_2 doi: 10.1128/jvi.69.10.6158-6169.1995 – ident: e_1_3_2_10_2 doi: 10.1006/cyto.2000.0797 – ident: e_1_3_2_12_2 doi: 10.1016/j.jss.2005.12.011 – ident: e_1_3_2_14_2 doi: 10.1111/j.1440-1746.2010.06539.x – ident: e_1_3_2_9_2 doi: 10.1038/cr.2010.183 – reference: 11145844 - Cytokine. 2001 Jan 7;13(1):60-64 – reference: 9082986 - Science. 1997 Apr 4;276(5309):60-6 – reference: 11375418 - J Clin Invest. 2001 May;107(10):1285-92 – reference: 21187858 - Cell Res. 2011 Jan;21(1):159-68 – reference: 21829354 - PLoS Pathog. 2011 Jul;7(7):e1002159 – reference: 1415718 - Am J Physiol. 1992 Oct;263(4 Pt 1):G579-85 – reference: 21199532 - J Gastroenterol Hepatol. 2011 Jan;26 Suppl 1:203-12 – reference: 20607568 - J Hepatobiliary Pancreat Sci. 2011 Jan;18(1):13-22 – reference: 9151875 - J Virol. 1997 Jun;71(6):4804-8 – reference: 12374864 - Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13825-30 – reference: 20142477 - Proc Natl Acad Sci U S A. 2010 Mar 2;107(9):4383-8 – reference: 20657822 - PLoS Pathog. 2010;6(7):e1000986 – reference: 12746193 - J Invest Surg. 2003 Mar-Apr;16(2):99-102 – reference: 18158318 - J Exp Med. 2008 Jan 21;205(1):91-103 – reference: 18765289 - Semin Cell Dev Biol. 2008 Aug;19(4):311-8 – reference: 8964411 - Gastroenterology. 1996 Jun;110(6):1854-62 – reference: 11836439 - J Virol. 2002 Mar;76(5):2579-84 – reference: 12829809 - J Virol. 2003 Jul;77(14):7707-12 – reference: 16447274 - Hepatology. 2006 Feb;43(2 Suppl 1):S45-53 – reference: 7666518 - J Virol. 1995 Oct;69(10):6158-69 – reference: 16458925 - J Surg Res. 2006 Aug;134(2):238-51 |
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Mendeley... Hepatitis B virus (HBV) is a hepatotropic virus that can cause severe liver diseases. By conducting studies using four different transgenic mouse lines that... |
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| SubjectTerms | Animals Base Sequence Biological and medical sciences DNA, Viral - blood DNA, Viral - genetics Fundamental and applied biological sciences. Psychology Hepatectomy Hepatitis B virus - genetics Hepatitis B virus - pathogenicity Hepatitis B virus - physiology Hepatocyte Nuclear Factor 3-gamma - metabolism Host-Pathogen Interactions - physiology Interferon-alpha - antagonists & inhibitors Interferon-alpha - physiology Interferon-beta - antagonists & inhibitors Interferon-beta - physiology Liver - injuries Liver - physiopathology Liver - virology Liver Regeneration - physiology Male Mice Mice, Inbred C57BL Mice, Transgenic Microbiology Miscellaneous STAT3 Transcription Factor - metabolism Suppressor of Cytokine Signaling 3 Protein Suppressor of Cytokine Signaling Proteins - metabolism Trans-Activators - genetics Trans-Activators - physiology Viral Load Virology Virus Replication Virus-Cell Interactions |
| Title | Viral-Load-Dependent Effects of Liver Injury and Regeneration on Hepatitis B Virus Replication in Mice |
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