Impact of the Interaction of Hepatitis B Virus with Mitochondria and Associated Proteins
Identifieur interne : 000976 ( Ncbi/Merge ); précédent : 000975; suivant : 000977Impact of the Interaction of Hepatitis B Virus with Mitochondria and Associated Proteins
Auteurs : Md. Golzar Hossain [Bangladesh] ; Sharmin Akter ; Eriko Ohsaki ; Keiji UedaSource :
- Viruses [ 1999-4915 ] ; 2020.
Abstract
Around 350 million people are living with hepatitis B virus (HBV), which can lead to death due to liver cirrhosis and hepatocellular carcinoma (HCC). Various antiviral drugs/nucleot(s)ide analogues are currently used to reduce or arrest the replication of this virus. However, many studies have reported that nucleot(s)ide analogue-resistant HBV is circulating. Cellular signaling pathways could be one of the targets against the viral replication. Several studies reported that viral proteins interacted with mitochondrial proteins and localized in the mitochondria, the powerhouse of the cell. And a recent study showed that mitochondrial turnover induced by thyroid hormones protected hepatocytes from hepatocarcinogenesis mediated by HBV. Strong downregulation of numerous cellular signaling pathways has also been reported to be accompanied by profound mitochondrial alteration, as confirmed by transcriptome profiling of HBV-specific CD8 T cells from chronic and acute HBV patients. In this review, we summarize the ongoing research into mitochondrial proteins and/or signaling involved with HBV proteins, which will continue to provide insight into the relationship between mitochondria and HBV and ultimately lead to advances in viral pathobiology and mitochondria-targeted antiviral therapy.
Url:
DOI: 10.3390/v12020175
PubMed: 32033216
PubMed Central: 7077294
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Impact of the Interaction of Hepatitis B Virus with Mitochondria and Associated Proteins</title><author><name sortKey="Hossain, Md Golzar" sort="Hossain, Md Golzar" uniqKey="Hossain M" first="Md. Golzar" last="Hossain">Md. Golzar Hossain</name><affiliation><nlm:aff id="af1-viruses-12-00175">Division of Virology, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan;<email>eohsaki@virus.med.osaka-u.ac.jp</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-viruses-12-00175">Department of Microbiology and Hygiene, Bangladesh Agricultural University, Mymensingh 2202, Bangladesh</nlm:aff><country xml:lang="fr">Bangladesh</country><wicri:regionArea>Department of Microbiology and Hygiene, Bangladesh Agricultural University, Mymensingh 2202</wicri:regionArea><wicri:noRegion>Mymensingh 2202</wicri:noRegion></affiliation></author><author><name sortKey="Akter, Sharmin" sort="Akter, Sharmin" uniqKey="Akter S" first="Sharmin" last="Akter">Sharmin Akter</name><affiliation><nlm:aff id="af3-viruses-12-00175">Department of Physiology, Bangladesh Agricultural University, Mymensingh 2202, Bangladesh;<email>sharmin.akter@bau.edu.bd</email></nlm:aff></affiliation></author><author><name sortKey="Ohsaki, Eriko" sort="Ohsaki, Eriko" uniqKey="Ohsaki E" first="Eriko" last="Ohsaki">Eriko Ohsaki</name><affiliation><nlm:aff id="af1-viruses-12-00175">Division of Virology, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan;<email>eohsaki@virus.med.osaka-u.ac.jp</email></nlm:aff></affiliation></author><author><name sortKey="Ueda, Keiji" sort="Ueda, Keiji" uniqKey="Ueda K" first="Keiji" last="Ueda">Keiji Ueda</name><affiliation><nlm:aff id="af1-viruses-12-00175">Division of Virology, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan;<email>eohsaki@virus.med.osaka-u.ac.jp</email></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">32033216</idno><idno type="pmc">7077294</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7077294</idno><idno type="RBID">PMC:7077294</idno><idno type="doi">10.3390/v12020175</idno><date when="2020">2020</date><idno type="wicri:Area/Pmc/Corpus">000B37</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000B37</idno><idno type="wicri:Area/Pmc/Curation">000B37</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000B37</idno><idno type="wicri:Area/Pmc/Checkpoint">000112</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000112</idno><idno type="wicri:Area/Ncbi/Merge">000976</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Impact of the Interaction of Hepatitis B Virus with Mitochondria and Associated Proteins</title><author><name sortKey="Hossain, Md Golzar" sort="Hossain, Md Golzar" uniqKey="Hossain M" first="Md. Golzar" last="Hossain">Md. Golzar Hossain</name><affiliation><nlm:aff id="af1-viruses-12-00175">Division of Virology, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan;<email>eohsaki@virus.med.osaka-u.ac.jp</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-viruses-12-00175">Department of Microbiology and Hygiene, Bangladesh Agricultural University, Mymensingh 2202, Bangladesh</nlm:aff><country xml:lang="fr">Bangladesh</country><wicri:regionArea>Department of Microbiology and Hygiene, Bangladesh Agricultural University, Mymensingh 2202</wicri:regionArea><wicri:noRegion>Mymensingh 2202</wicri:noRegion></affiliation></author><author><name sortKey="Akter, Sharmin" sort="Akter, Sharmin" uniqKey="Akter S" first="Sharmin" last="Akter">Sharmin Akter</name><affiliation><nlm:aff id="af3-viruses-12-00175">Department of Physiology, Bangladesh Agricultural University, Mymensingh 2202, Bangladesh;<email>sharmin.akter@bau.edu.bd</email></nlm:aff></affiliation></author><author><name sortKey="Ohsaki, Eriko" sort="Ohsaki, Eriko" uniqKey="Ohsaki E" first="Eriko" last="Ohsaki">Eriko Ohsaki</name><affiliation><nlm:aff id="af1-viruses-12-00175">Division of Virology, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan;<email>eohsaki@virus.med.osaka-u.ac.jp</email></nlm:aff></affiliation></author><author><name sortKey="Ueda, Keiji" sort="Ueda, Keiji" uniqKey="Ueda K" first="Keiji" last="Ueda">Keiji Ueda</name><affiliation><nlm:aff id="af1-viruses-12-00175">Division of Virology, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan;<email>eohsaki@virus.med.osaka-u.ac.jp</email></nlm:aff></affiliation></author></analytic><series><title level="j">Viruses</title><idno type="eISSN">1999-4915</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Around 350 million people are living with hepatitis B virus (HBV), which can lead to death due to liver cirrhosis and hepatocellular carcinoma (HCC). Various antiviral drugs/nucleot(s)ide analogues are currently used to reduce or arrest the replication of this virus. However, many studies have reported that nucleot(s)ide analogue-resistant HBV is circulating. Cellular signaling pathways could be one of the targets against the viral replication. Several studies reported that viral proteins interacted with mitochondrial proteins and localized in the mitochondria, the powerhouse of the cell. And a recent study showed that mitochondrial turnover induced by thyroid hormones protected hepatocytes from hepatocarcinogenesis mediated by HBV. Strong downregulation of numerous cellular signaling pathways has also been reported to be accompanied by profound mitochondrial alteration, as confirmed by transcriptome profiling of HBV-specific CD8 T cells from chronic and acute HBV patients. In this review, we summarize the ongoing research into mitochondrial proteins and/or signaling involved with HBV proteins, which will continue to provide insight into the relationship between mitochondria and HBV and ultimately lead to advances in viral pathobiology and mitochondria-targeted antiviral therapy.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Endo, T" uniqKey="Endo T">T. Endo</name></author><author><name sortKey="Yamano, K" uniqKey="Yamano K">K. Yamano</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, C" uniqKey="Wang C">C. Wang</name></author><author><name sortKey="Youle, R J" uniqKey="Youle R">R.J. Youle</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hayashi, T" uniqKey="Hayashi T">T. Hayashi</name></author><author><name sortKey="Rizzuto, R" uniqKey="Rizzuto R">R. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Viruses</journal-id><journal-id journal-id-type="iso-abbrev">Viruses</journal-id><journal-id journal-id-type="publisher-id">viruses</journal-id><journal-title-group><journal-title>Viruses</journal-title></journal-title-group><issn pub-type="epub">1999-4915</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">32033216</article-id><article-id pub-id-type="pmc">7077294</article-id><article-id pub-id-type="doi">10.3390/v12020175</article-id><article-id pub-id-type="publisher-id">viruses-12-00175</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Impact of the Interaction of Hepatitis B Virus with Mitochondria and Associated Proteins</article-title></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0002-1487-5444</contrib-id><name><surname>Hossain</surname><given-names>Md. Golzar</given-names></name><xref ref-type="aff" rid="af1-viruses-12-00175">1</xref><xref ref-type="aff" rid="af2-viruses-12-00175">2</xref><xref rid="c1-viruses-12-00175" ref-type="corresp">*</xref></contrib><contrib contrib-type="author"><name><surname>Akter</surname><given-names>Sharmin</given-names></name><xref ref-type="aff" rid="af3-viruses-12-00175">3</xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0002-1496-0964</contrib-id><name><surname>Ohsaki</surname><given-names>Eriko</given-names></name><xref ref-type="aff" rid="af1-viruses-12-00175">1</xref></contrib><contrib contrib-type="author"><name><surname>Ueda</surname><given-names>Keiji</given-names></name><xref ref-type="aff" rid="af1-viruses-12-00175">1</xref><xref rid="c1-viruses-12-00175" ref-type="corresp">*</xref></contrib></contrib-group><aff id="af1-viruses-12-00175"><label>1</label>Division of Virology, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan;<email>eohsaki@virus.med.osaka-u.ac.jp</email></aff><aff id="af2-viruses-12-00175"><label>2</label>Department of Microbiology and Hygiene, Bangladesh Agricultural University, Mymensingh 2202, Bangladesh</aff><aff id="af3-viruses-12-00175"><label>3</label>Department of Physiology, Bangladesh Agricultural University, Mymensingh 2202, Bangladesh;<email>sharmin.akter@bau.edu.bd</email></aff><author-notes><corresp id="c1-viruses-12-00175"><label>*</label>Correspondence: <email>mghossain@bau.edu.bd</email> (M.G.H.); <email>kueda@virus.med.osaka-u.ac.jp</email> (K.U.)</corresp></author-notes><pub-date pub-type="epub"><day>04</day><month>2</month><year>2020</year></pub-date><pub-date pub-type="collection"><month>2</month><year>2020</year></pub-date><volume>12</volume><issue>2</issue><elocation-id>175</elocation-id><history><date date-type="received"><day>16</day><month>12</month><year>2019</year></date><date date-type="accepted"><day>03</day><month>2</month><year>2020</year></date></history><permissions><copyright-statement>© 2020 by the authors.</copyright-statement><copyright-year>2020</copyright-year><license license-type="open-access"><license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>).</license-p></license></permissions><abstract><p>Around 350 million people are living with hepatitis B virus (HBV), which can lead to death due to liver cirrhosis and hepatocellular carcinoma (HCC). Various antiviral drugs/nucleot(s)ide analogues are currently used to reduce or arrest the replication of this virus. However, many studies have reported that nucleot(s)ide analogue-resistant HBV is circulating. Cellular signaling pathways could be one of the targets against the viral replication. Several studies reported that viral proteins interacted with mitochondrial proteins and localized in the mitochondria, the powerhouse of the cell. And a recent study showed that mitochondrial turnover induced by thyroid hormones protected hepatocytes from hepatocarcinogenesis mediated by HBV. Strong downregulation of numerous cellular signaling pathways has also been reported to be accompanied by profound mitochondrial alteration, as confirmed by transcriptome profiling of HBV-specific CD8 T cells from chronic and acute HBV patients. In this review, we summarize the ongoing research into mitochondrial proteins and/or signaling involved with HBV proteins, which will continue to provide insight into the relationship between mitochondria and HBV and ultimately lead to advances in viral pathobiology and mitochondria-targeted antiviral therapy.</p></abstract><kwd-group><kwd>Hepatitis B virus (HBV)</kwd><kwd>mitochondria</kwd><kwd>proteins/signaling</kwd><kwd>interaction</kwd></kwd-group></article-meta></front><floats-group><fig id="viruses-12-00175-f001" orientation="portrait" position="float"><label>Figure 1</label><caption><p>Hepatitis B virus (HBV) genomic map and an overview of the HBV life cycle. (<bold>A</bold>). HBV genomic map. The partially double-stranded DNA encodes four overlapping open reading frames (ORFs), preC-C, P, preS-S, and X. The ORF P overlaps the other three open reading frames (ORFs). (<bold>B</bold>). An overview of the HBV life cycle. HBV infects hepatocytes through preS1-NTCP interaction followed by uncoating and is transported to the nucleus where cccDNA is formed. The cccDNA acts as a template for transcription of the 3.5 kb pregenomic RNA (pgRNA), and the 2.4 kb, 2.1 kb, and 0.7 kb subgenomic RNAs. The pol translated from pgRNA is encapsidated along with pgRNA, then reverse-transcribed, and the partially double-stranded DNA genome is formed. The core particle is enveloped in ER-Golgi/MVB and secreted into the extracellular space.</p></caption><graphic xlink:href="viruses-12-00175-g001"></graphic></fig><fig id="viruses-12-00175-f002" orientation="portrait" position="float"><label>Figure 2</label><caption><p>Interactions between HBV proteins and mitochondrial proteins. HBx interacts with different mitochondrial proteins and/or translocates several cytosolic proteins into mitochondria, which affects mitochondrial fission, morphology, and biogenesis and leads to mitophagy/dysfunction. Innate immunity is lost due to decreased activities of IRF3 and IFN-β through MAVS/parkin/HBx interaction. Cell death/apoptosis may occur due to loss of Δψm and release of cytochrome c induced by HBx. Increase in mROS due to HBx causes mtDNA destruction and activation of oncogenic transcription factors, which might lead to HCC development. Pol interacts with STING and reduces the antiviral immunity through suppression of IFN-β. HBsAg interacts with and degrades GRP78 and up-regulates IFN-β to suppress HBV replication. Viral replication is also suppressed by degradation of HBc and HBx through interaction between HBc and hTid1. HBx translocates Raf1 into mitochondria. HBsAg binds with JTB and reduces the mitochondrial localization of JTB. Double arrows indicate interactions and dashed arrows indicate translocations.</p></caption><graphic xlink:href="viruses-12-00175-g002"></graphic></fig></floats-group></pmc><affiliations><list><country><li>Bangladesh</li></country></list><tree><noCountry><name sortKey="Akter, Sharmin" sort="Akter, Sharmin" uniqKey="Akter S" first="Sharmin" last="Akter">Sharmin Akter</name><name sortKey="Ohsaki, Eriko" sort="Ohsaki, Eriko" uniqKey="Ohsaki E" first="Eriko" last="Ohsaki">Eriko Ohsaki</name><name sortKey="Ueda, Keiji" sort="Ueda, Keiji" uniqKey="Ueda K" first="Keiji" last="Ueda">Keiji Ueda</name></noCountry><country name="Bangladesh"><noRegion><name sortKey="Hossain, Md Golzar" sort="Hossain, Md Golzar" uniqKey="Hossain M" first="Md. Golzar" last="Hossain">Md. Golzar Hossain</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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