Activation of the Liver X Receptor Pathway Inhibits HBV Replication in Primary Human Hepatocytes
Background and Aims Hepatitis B virus (HBV) infection is ranked among the top health priorities worldwide. Accumulating evidence suggests that HBV infection and replication are closely associated with liver metabolism. The liver X receptors (LXRs), which belong to the superfamily of nuclear hormone...
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| Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 2020-12, Vol.72 (6), p.1935-1948 |
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| container_issue | 6 |
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| container_title | Hepatology (Baltimore, Md.) |
| container_volume | 72 |
| creator | Zeng, Jing Wu, Daitze Hu, Hui Young, John A.T. Yan, Zhipeng Gao, Lu |
| description | Background and Aims
Hepatitis B virus (HBV) infection is ranked among the top health priorities worldwide. Accumulating evidence suggests that HBV infection and replication are closely associated with liver metabolism. The liver X receptors (LXRs), which belong to the superfamily of nuclear hormone receptors, are important physiological regulators of lipid and cholesterol metabolism. However, the association between the LXR pathway and HBV infection remains largely unclear.
Approach and Results
In this study, the antiviral activity of LXR agonists was investigated using multiple HBV cellular models. We observed that in HBV‐infected primary human hepatocytes (PHHs), synthetic LXR agonists (T0901317, GW3965, and LXR‐623), but not an LXR antagonist (SR9238), potently inhibited HBV replication and gene expression, as demonstrated by substantial reductions in viral RNA, DNA, and antigen production following agonist treatment. However, covalently closed circular DNA (cccDNA) levels were not significantly reduced by the agonists. In addition, no rebound in viral replication was observed after treatment withdrawal, indicating a long‐lasting inhibitory effect. These results suggest that LXR agonists decrease the transcriptional activity of cccDNA. In contrast, no significant anti‐HBV effect was observed in HepG2‐derived cell lines. Interestingly, LXR agonist treatment strongly reduced cholesterol 7α‐hydroxylase 1 (CYP7A1) mRNA levels. Knockdown of CYP7A1 gene expression with small interfering RNA inhibited HBV activity in PHHs, suggesting CYP7A1 as a potential factor contributing to the antiviral effects of LXR agonists.
Conclusions
We found that activation of the LXR pathway with synthetic LXR agonists could elicit potent anti‐HBV activity in PHHs, possibly through sustained suppression of cccDNA transcription. Our work highlights the therapeutic potential of targeting the LXR pathway for the treatment of chronic HBV infection. |
| doi_str_mv | 10.1002/hep.31217 |
| format | Article |
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Hepatitis B virus (HBV) infection is ranked among the top health priorities worldwide. Accumulating evidence suggests that HBV infection and replication are closely associated with liver metabolism. The liver X receptors (LXRs), which belong to the superfamily of nuclear hormone receptors, are important physiological regulators of lipid and cholesterol metabolism. However, the association between the LXR pathway and HBV infection remains largely unclear.
Approach and Results
In this study, the antiviral activity of LXR agonists was investigated using multiple HBV cellular models. We observed that in HBV‐infected primary human hepatocytes (PHHs), synthetic LXR agonists (T0901317, GW3965, and LXR‐623), but not an LXR antagonist (SR9238), potently inhibited HBV replication and gene expression, as demonstrated by substantial reductions in viral RNA, DNA, and antigen production following agonist treatment. However, covalently closed circular DNA (cccDNA) levels were not significantly reduced by the agonists. In addition, no rebound in viral replication was observed after treatment withdrawal, indicating a long‐lasting inhibitory effect. These results suggest that LXR agonists decrease the transcriptional activity of cccDNA. In contrast, no significant anti‐HBV effect was observed in HepG2‐derived cell lines. Interestingly, LXR agonist treatment strongly reduced cholesterol 7α‐hydroxylase 1 (CYP7A1) mRNA levels. Knockdown of CYP7A1 gene expression with small interfering RNA inhibited HBV activity in PHHs, suggesting CYP7A1 as a potential factor contributing to the antiviral effects of LXR agonists.
Conclusions
We found that activation of the LXR pathway with synthetic LXR agonists could elicit potent anti‐HBV activity in PHHs, possibly through sustained suppression of cccDNA transcription. Our work highlights the therapeutic potential of targeting the LXR pathway for the treatment of chronic HBV infection.</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.31217</identifier><identifier>PMID: 32145089</identifier><language>eng</language><publisher>United States: Wolters Kluwer Health, Inc</publisher><subject>Agonists ; Antigens, Viral - genetics ; Antigens, Viral - isolation & purification ; Antiviral activity ; Antiviral Agents - pharmacology ; Antiviral Agents - therapeutic use ; Benzoates - pharmacology ; Benzoates - therapeutic use ; Benzylamines - pharmacology ; Benzylamines - therapeutic use ; Cell lines ; Cells, Cultured ; Cholesterol ; Cholesterol 7-alpha-Hydroxylase - genetics ; Cholesterol 7-alpha-Hydroxylase - metabolism ; Chronic infection ; Circular DNA ; CYP7A1 gene ; Deoxyribonucleic acid ; DNA ; DNA, Viral - isolation & purification ; Drug Evaluation, Preclinical ; Gene expression ; Gene Knockdown Techniques ; Hepatitis B ; Hepatitis B - drug therapy ; Hepatitis B - virology ; Hepatitis B virus - drug effects ; Hepatitis B virus - physiology ; Hepatocytes ; Hepatology ; Heterocyclic Compounds, 4 or More Rings - pharmacology ; Humans ; Hydrocarbons, Fluorinated - pharmacology ; Hydrocarbons, Fluorinated - therapeutic use ; Hydroxylase ; Indazoles - pharmacology ; Indazoles - therapeutic use ; Infections ; Lipid metabolism ; Liver - cytology ; Liver - metabolism ; Liver X receptors ; Liver X Receptors - agonists ; Liver X Receptors - antagonists & inhibitors ; Liver X Receptors - metabolism ; Metabolism ; Nuclear receptors ; Primary Cell Culture ; Replication ; RNA, Viral - isolation & purification ; Signal Transduction - drug effects ; siRNA ; Sulfonamides - pharmacology ; Sulfonamides - therapeutic use ; Transcription ; Virus Replication - drug effects</subject><ispartof>Hepatology (Baltimore, Md.), 2020-12, Vol.72 (6), p.1935-1948</ispartof><rights>2020 by the American Association for the Study of Liver Diseases.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3537-3934d4e43238aa1cf3fd7d95998562c97e2d9a3dab14803e898816e8202df6a13</citedby><cites>FETCH-LOGICAL-c3537-3934d4e43238aa1cf3fd7d95998562c97e2d9a3dab14803e898816e8202df6a13</cites><orcidid>0000-0002-8463-1891</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhep.31217$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhep.31217$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32145089$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zeng, Jing</creatorcontrib><creatorcontrib>Wu, Daitze</creatorcontrib><creatorcontrib>Hu, Hui</creatorcontrib><creatorcontrib>Young, John A.T.</creatorcontrib><creatorcontrib>Yan, Zhipeng</creatorcontrib><creatorcontrib>Gao, Lu</creatorcontrib><title>Activation of the Liver X Receptor Pathway Inhibits HBV Replication in Primary Human Hepatocytes</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>Background and Aims
Hepatitis B virus (HBV) infection is ranked among the top health priorities worldwide. Accumulating evidence suggests that HBV infection and replication are closely associated with liver metabolism. The liver X receptors (LXRs), which belong to the superfamily of nuclear hormone receptors, are important physiological regulators of lipid and cholesterol metabolism. However, the association between the LXR pathway and HBV infection remains largely unclear.
Approach and Results
In this study, the antiviral activity of LXR agonists was investigated using multiple HBV cellular models. We observed that in HBV‐infected primary human hepatocytes (PHHs), synthetic LXR agonists (T0901317, GW3965, and LXR‐623), but not an LXR antagonist (SR9238), potently inhibited HBV replication and gene expression, as demonstrated by substantial reductions in viral RNA, DNA, and antigen production following agonist treatment. However, covalently closed circular DNA (cccDNA) levels were not significantly reduced by the agonists. In addition, no rebound in viral replication was observed after treatment withdrawal, indicating a long‐lasting inhibitory effect. These results suggest that LXR agonists decrease the transcriptional activity of cccDNA. In contrast, no significant anti‐HBV effect was observed in HepG2‐derived cell lines. Interestingly, LXR agonist treatment strongly reduced cholesterol 7α‐hydroxylase 1 (CYP7A1) mRNA levels. Knockdown of CYP7A1 gene expression with small interfering RNA inhibited HBV activity in PHHs, suggesting CYP7A1 as a potential factor contributing to the antiviral effects of LXR agonists.
Conclusions
We found that activation of the LXR pathway with synthetic LXR agonists could elicit potent anti‐HBV activity in PHHs, possibly through sustained suppression of cccDNA transcription. Our work highlights the therapeutic potential of targeting the LXR pathway for the treatment of chronic HBV infection.</description><subject>Agonists</subject><subject>Antigens, Viral - genetics</subject><subject>Antigens, Viral - isolation & purification</subject><subject>Antiviral activity</subject><subject>Antiviral Agents - pharmacology</subject><subject>Antiviral Agents - therapeutic use</subject><subject>Benzoates - pharmacology</subject><subject>Benzoates - therapeutic use</subject><subject>Benzylamines - pharmacology</subject><subject>Benzylamines - therapeutic use</subject><subject>Cell lines</subject><subject>Cells, Cultured</subject><subject>Cholesterol</subject><subject>Cholesterol 7-alpha-Hydroxylase - genetics</subject><subject>Cholesterol 7-alpha-Hydroxylase - metabolism</subject><subject>Chronic infection</subject><subject>Circular DNA</subject><subject>CYP7A1 gene</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA, Viral - isolation & purification</subject><subject>Drug Evaluation, Preclinical</subject><subject>Gene expression</subject><subject>Gene Knockdown Techniques</subject><subject>Hepatitis B</subject><subject>Hepatitis B - drug therapy</subject><subject>Hepatitis B - virology</subject><subject>Hepatitis B virus - drug effects</subject><subject>Hepatitis B virus - physiology</subject><subject>Hepatocytes</subject><subject>Hepatology</subject><subject>Heterocyclic Compounds, 4 or More Rings - pharmacology</subject><subject>Humans</subject><subject>Hydrocarbons, Fluorinated - pharmacology</subject><subject>Hydrocarbons, Fluorinated - therapeutic use</subject><subject>Hydroxylase</subject><subject>Indazoles - pharmacology</subject><subject>Indazoles - therapeutic use</subject><subject>Infections</subject><subject>Lipid metabolism</subject><subject>Liver - cytology</subject><subject>Liver - metabolism</subject><subject>Liver X receptors</subject><subject>Liver X Receptors - agonists</subject><subject>Liver X Receptors - antagonists & inhibitors</subject><subject>Liver X Receptors - metabolism</subject><subject>Metabolism</subject><subject>Nuclear receptors</subject><subject>Primary Cell Culture</subject><subject>Replication</subject><subject>RNA, Viral - isolation & purification</subject><subject>Signal Transduction - drug effects</subject><subject>siRNA</subject><subject>Sulfonamides - pharmacology</subject><subject>Sulfonamides - therapeutic use</subject><subject>Transcription</subject><subject>Virus Replication - drug effects</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1rGzEQhkVpaZyPQ_9AEfTSHJxIGq1XOqbGyQYMMSUJuamydhYrrHe3K62N_33VbppDIIdhDvPMw8xLyBfOLjhj4nKD3QVwwfMPZMIzkU8BMvaRTJjI2VRz0EfkOIRnxpiWQn0mRyC4zJjSE_LrykW_s9G3DW0rGjdIl36HPX2iP9FhF9uermzc7O2B3jYbv_Yx0OLHY5p2tXfjom_oqvdb2x9oMWxtQwvsbGzdIWI4JZ8qWwc8e-kn5OF6cT8vpsu7m9v51XLqIIN0sQZZSpQgQFnLXQVVmZc601plM-F0jqLUFkq75lIxQKWV4jNUgomymlkOJ-T76O369veAIZqtDw7r2jbYDsEIyCVIAJ4l9Nsb9Lkd-iZdZ4TMRSoOs0Sdj5Tr2xB6rEw3_mg4M39jNyl28y_2xH59MQ7rLZav5P-cE3A5Antf4-F9kykWq1H5B9_KihY</recordid><startdate>202012</startdate><enddate>202012</enddate><creator>Zeng, Jing</creator><creator>Wu, Daitze</creator><creator>Hu, Hui</creator><creator>Young, John A.T.</creator><creator>Yan, Zhipeng</creator><creator>Gao, Lu</creator><general>Wolters Kluwer Health, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8463-1891</orcidid></search><sort><creationdate>202012</creationdate><title>Activation of the Liver X Receptor Pathway Inhibits HBV Replication in Primary Human Hepatocytes</title><author>Zeng, Jing ; Wu, Daitze ; Hu, Hui ; Young, John A.T. ; Yan, Zhipeng ; Gao, Lu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3537-3934d4e43238aa1cf3fd7d95998562c97e2d9a3dab14803e898816e8202df6a13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Agonists</topic><topic>Antigens, Viral - genetics</topic><topic>Antigens, Viral - isolation & purification</topic><topic>Antiviral activity</topic><topic>Antiviral Agents - pharmacology</topic><topic>Antiviral Agents - therapeutic use</topic><topic>Benzoates - pharmacology</topic><topic>Benzoates - therapeutic use</topic><topic>Benzylamines - pharmacology</topic><topic>Benzylamines - therapeutic use</topic><topic>Cell lines</topic><topic>Cells, Cultured</topic><topic>Cholesterol</topic><topic>Cholesterol 7-alpha-Hydroxylase - genetics</topic><topic>Cholesterol 7-alpha-Hydroxylase - metabolism</topic><topic>Chronic infection</topic><topic>Circular DNA</topic><topic>CYP7A1 gene</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA, Viral - isolation & purification</topic><topic>Drug Evaluation, Preclinical</topic><topic>Gene expression</topic><topic>Gene Knockdown Techniques</topic><topic>Hepatitis B</topic><topic>Hepatitis B - drug therapy</topic><topic>Hepatitis B - virology</topic><topic>Hepatitis B virus - drug effects</topic><topic>Hepatitis B virus - physiology</topic><topic>Hepatocytes</topic><topic>Hepatology</topic><topic>Heterocyclic Compounds, 4 or More Rings - pharmacology</topic><topic>Humans</topic><topic>Hydrocarbons, Fluorinated - pharmacology</topic><topic>Hydrocarbons, Fluorinated - therapeutic use</topic><topic>Hydroxylase</topic><topic>Indazoles - pharmacology</topic><topic>Indazoles - therapeutic use</topic><topic>Infections</topic><topic>Lipid metabolism</topic><topic>Liver - cytology</topic><topic>Liver - metabolism</topic><topic>Liver X receptors</topic><topic>Liver X Receptors - agonists</topic><topic>Liver X Receptors - antagonists & inhibitors</topic><topic>Liver X Receptors - metabolism</topic><topic>Metabolism</topic><topic>Nuclear receptors</topic><topic>Primary Cell Culture</topic><topic>Replication</topic><topic>RNA, Viral - isolation & purification</topic><topic>Signal Transduction - drug effects</topic><topic>siRNA</topic><topic>Sulfonamides - pharmacology</topic><topic>Sulfonamides - therapeutic use</topic><topic>Transcription</topic><topic>Virus Replication - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zeng, Jing</creatorcontrib><creatorcontrib>Wu, Daitze</creatorcontrib><creatorcontrib>Hu, Hui</creatorcontrib><creatorcontrib>Young, John A.T.</creatorcontrib><creatorcontrib>Yan, Zhipeng</creatorcontrib><creatorcontrib>Gao, Lu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeng, Jing</au><au>Wu, Daitze</au><au>Hu, Hui</au><au>Young, John A.T.</au><au>Yan, Zhipeng</au><au>Gao, Lu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of the Liver X Receptor Pathway Inhibits HBV Replication in Primary Human Hepatocytes</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>2020-12</date><risdate>2020</risdate><volume>72</volume><issue>6</issue><spage>1935</spage><epage>1948</epage><pages>1935-1948</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><abstract>Background and Aims
Hepatitis B virus (HBV) infection is ranked among the top health priorities worldwide. Accumulating evidence suggests that HBV infection and replication are closely associated with liver metabolism. The liver X receptors (LXRs), which belong to the superfamily of nuclear hormone receptors, are important physiological regulators of lipid and cholesterol metabolism. However, the association between the LXR pathway and HBV infection remains largely unclear.
Approach and Results
In this study, the antiviral activity of LXR agonists was investigated using multiple HBV cellular models. We observed that in HBV‐infected primary human hepatocytes (PHHs), synthetic LXR agonists (T0901317, GW3965, and LXR‐623), but not an LXR antagonist (SR9238), potently inhibited HBV replication and gene expression, as demonstrated by substantial reductions in viral RNA, DNA, and antigen production following agonist treatment. However, covalently closed circular DNA (cccDNA) levels were not significantly reduced by the agonists. In addition, no rebound in viral replication was observed after treatment withdrawal, indicating a long‐lasting inhibitory effect. These results suggest that LXR agonists decrease the transcriptional activity of cccDNA. In contrast, no significant anti‐HBV effect was observed in HepG2‐derived cell lines. Interestingly, LXR agonist treatment strongly reduced cholesterol 7α‐hydroxylase 1 (CYP7A1) mRNA levels. Knockdown of CYP7A1 gene expression with small interfering RNA inhibited HBV activity in PHHs, suggesting CYP7A1 as a potential factor contributing to the antiviral effects of LXR agonists.
Conclusions
We found that activation of the LXR pathway with synthetic LXR agonists could elicit potent anti‐HBV activity in PHHs, possibly through sustained suppression of cccDNA transcription. Our work highlights the therapeutic potential of targeting the LXR pathway for the treatment of chronic HBV infection.</abstract><cop>United States</cop><pub>Wolters Kluwer Health, Inc</pub><pmid>32145089</pmid><doi>10.1002/hep.31217</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-8463-1891</orcidid></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Agonists Antigens, Viral - genetics Antigens, Viral - isolation & purification Antiviral activity Antiviral Agents - pharmacology Antiviral Agents - therapeutic use Benzoates - pharmacology Benzoates - therapeutic use Benzylamines - pharmacology Benzylamines - therapeutic use Cell lines Cells, Cultured Cholesterol Cholesterol 7-alpha-Hydroxylase - genetics Cholesterol 7-alpha-Hydroxylase - metabolism Chronic infection Circular DNA CYP7A1 gene Deoxyribonucleic acid DNA DNA, Viral - isolation & purification Drug Evaluation, Preclinical Gene expression Gene Knockdown Techniques Hepatitis B Hepatitis B - drug therapy Hepatitis B - virology Hepatitis B virus - drug effects Hepatitis B virus - physiology Hepatocytes Hepatology Heterocyclic Compounds, 4 or More Rings - pharmacology Humans Hydrocarbons, Fluorinated - pharmacology Hydrocarbons, Fluorinated - therapeutic use Hydroxylase Indazoles - pharmacology Indazoles - therapeutic use Infections Lipid metabolism Liver - cytology Liver - metabolism Liver X receptors Liver X Receptors - agonists Liver X Receptors - antagonists & inhibitors Liver X Receptors - metabolism Metabolism Nuclear receptors Primary Cell Culture Replication RNA, Viral - isolation & purification Signal Transduction - drug effects siRNA Sulfonamides - pharmacology Sulfonamides - therapeutic use Transcription Virus Replication - drug effects |
| title | Activation of the Liver X Receptor Pathway Inhibits HBV Replication in Primary Human Hepatocytes |
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