Hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1-mediated viral RNA editing in hepatocytes
HBV is considered as a “stealth” virus that does not invoke interferon (IFN) responses; however, the mechanisms by which HBV bypasses innate immune recognition are poorly understood. In this study, we identified adenosine deaminases acting on RNA 1 (ADAR1), which is a key factor in HBV evasion from...
Gespeichert in:
| Veröffentlicht in: | Cellular & molecular immunology 2021-08, Vol.18 (8), p.1871-1882 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1882 |
|---|---|
| container_issue | 8 |
| container_start_page | 1871 |
| container_title | Cellular & molecular immunology |
| container_volume | 18 |
| creator | Wang, Liyuan Sun, Yang Song, Xiaojia Wang, Zehua Zhang, Yankun Zhao, Ying Peng, Xueqi Zhang, Xiaodong Li, Chunyang Gao, Chengjiang Li, Nailin Gao, Lifen Liang, Xiaohong Wu, Zhuanchang Ma, Chunhong |
| description | HBV is considered as a “stealth” virus that does not invoke interferon (IFN) responses; however, the mechanisms by which HBV bypasses innate immune recognition are poorly understood. In this study, we identified adenosine deaminases acting on RNA 1 (ADAR1), which is a key factor in HBV evasion from IFN responses in hepatocytes. Mechanically, ADAR1 interacted with HBV RNAs and deaminated adenosine (A) to generate inosine (I), which disrupted host immune recognition and thus promoted HBV replication. Loss of ADAR1 or its deficient deaminase activity promoted IFN responses and inhibited HBV replication in hepatocytes, and blocking the IFN signaling pathways released the inhibition of HBV replication caused by ADAR1 deficiency. Notably, the HBV X protein (HBx) transcriptionally promoted ADAR1 expression to increase the threshold required to trigger intrinsic immune activation, which in turn enhanced HBV escape from immune recognition, leading to persistent infection. Supplementation with 8-azaadenosine, an ADAR1 inhibitor, efficiently enhanced liver immune activation to promote HBV clearance in vivo and in vitro. Taken together, our results delineate a molecular mechanism by which HBx promotes ADAR1-derived HBV immune escape and suggest a targeted therapeutic intervention for HBV infection. |
| doi_str_mv | 10.1038/s41423-021-00729-1 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_swepu</sourceid><recordid>TN_cdi_swepub_primary_oai_swepub_ki_se_460546</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2556149169</sourcerecordid><originalsourceid>FETCH-LOGICAL-c512t-eb66d98abbc288e673182058bc8ff17f7e99db943697269757e7ce23354dbf2c3</originalsourceid><addsrcrecordid>eNp9kktv1DAUhS0EokPhD7BAltiwSfErtrNBGsqjSBVIFawtx7mZukzsIU6m6r_nTmdaKAsWVqx7vnucY19CXnJ2wpm0b4viSsiKCV4xZkRT8UdkIZgSWBL6MVlwbURltOVH5FkpV4zVVhn1lBxJJWpp62ZBrs9g46c4xULf020c50Jh6zsoNA7DnICOEPIqIZAT6p5efF1S1FMuEdUO_BCTL0CXH5YXvBqgi36Cbmfl17cwVqaYVjQmerk7K4ebCcpz8qT36wIvDt9j8uPTx--nZ9X5t89fTpfnVai5mCpote4a69s2CGtBG8mtwBhtsH3PTW-gabq2UVI3RuCqDZgAQspadW0vgjwm1d63XMNmbt1mjIMfb1z20R1KP3EHTmlWK438uz2PCoYJkCYM8qDtoZLipVvlrbNSCHwENHhzMBjzrxnK5IZYAqzXPkGeixM1BuNM8wbR1_-gV3keE17HjtJcNVzvKLGnwphLGaG__xnO3G4O3H4OHM6Bu50Dx7Hp1d8x7lvuHh4BebgXlNIKxj9n_8f2N1ZVv2E</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2556149169</pqid></control><display><type>article</type><title>Hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1-mediated viral RNA editing in hepatocytes</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>SWEPUB Freely available online</source><creator>Wang, Liyuan ; Sun, Yang ; Song, Xiaojia ; Wang, Zehua ; Zhang, Yankun ; Zhao, Ying ; Peng, Xueqi ; Zhang, Xiaodong ; Li, Chunyang ; Gao, Chengjiang ; Li, Nailin ; Gao, Lifen ; Liang, Xiaohong ; Wu, Zhuanchang ; Ma, Chunhong</creator><creatorcontrib>Wang, Liyuan ; Sun, Yang ; Song, Xiaojia ; Wang, Zehua ; Zhang, Yankun ; Zhao, Ying ; Peng, Xueqi ; Zhang, Xiaodong ; Li, Chunyang ; Gao, Chengjiang ; Li, Nailin ; Gao, Lifen ; Liang, Xiaohong ; Wu, Zhuanchang ; Ma, Chunhong</creatorcontrib><description>HBV is considered as a “stealth” virus that does not invoke interferon (IFN) responses; however, the mechanisms by which HBV bypasses innate immune recognition are poorly understood. In this study, we identified adenosine deaminases acting on RNA 1 (ADAR1), which is a key factor in HBV evasion from IFN responses in hepatocytes. Mechanically, ADAR1 interacted with HBV RNAs and deaminated adenosine (A) to generate inosine (I), which disrupted host immune recognition and thus promoted HBV replication. Loss of ADAR1 or its deficient deaminase activity promoted IFN responses and inhibited HBV replication in hepatocytes, and blocking the IFN signaling pathways released the inhibition of HBV replication caused by ADAR1 deficiency. Notably, the HBV X protein (HBx) transcriptionally promoted ADAR1 expression to increase the threshold required to trigger intrinsic immune activation, which in turn enhanced HBV escape from immune recognition, leading to persistent infection. Supplementation with 8-azaadenosine, an ADAR1 inhibitor, efficiently enhanced liver immune activation to promote HBV clearance in vivo and in vitro. Taken together, our results delineate a molecular mechanism by which HBx promotes ADAR1-derived HBV immune escape and suggest a targeted therapeutic intervention for HBV infection.</description><identifier>ISSN: 1672-7681</identifier><identifier>ISSN: 2042-0226</identifier><identifier>EISSN: 2042-0226</identifier><identifier>DOI: 10.1038/s41423-021-00729-1</identifier><identifier>PMID: 34253859</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/250/254 ; 631/250/255/234/2513/1549 ; Adenosine ; Adenosine deaminase ; Adenosine Deaminase - genetics ; Adenosine Deaminase - metabolism ; Antibodies ; Biomedical and Life Sciences ; Biomedicine ; Hepatitis B ; Hepatitis B virus - metabolism ; Hepatocytes ; Hepatocytes - metabolism ; Immune clearance ; Immune response ; Immunology ; Interferon ; Medical Microbiology ; Microbiology ; Replication ; RNA Editing ; RNA, Viral - genetics ; RNA-Binding Proteins - metabolism ; Supplements ; Transcription ; Vaccine</subject><ispartof>Cellular & molecular immunology, 2021-08, Vol.18 (8), p.1871-1882</ispartof><rights>The Author(s), under exclusive licence to CSI and USTC 2021</rights><rights>2021. The Author(s), under exclusive licence to CSI and USTC.</rights><rights>The Author(s), under exclusive licence to CSI and USTC 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c512t-eb66d98abbc288e673182058bc8ff17f7e99db943697269757e7ce23354dbf2c3</citedby><cites>FETCH-LOGICAL-c512t-eb66d98abbc288e673182058bc8ff17f7e99db943697269757e7ce23354dbf2c3</cites><orcidid>0000-0002-5798-2274 ; 0000-0002-8121-4718 ; 0000-0002-9365-4497 ; 0000-0002-3848-7251</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8322072/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8322072/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,550,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34253859$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:147101991$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Liyuan</creatorcontrib><creatorcontrib>Sun, Yang</creatorcontrib><creatorcontrib>Song, Xiaojia</creatorcontrib><creatorcontrib>Wang, Zehua</creatorcontrib><creatorcontrib>Zhang, Yankun</creatorcontrib><creatorcontrib>Zhao, Ying</creatorcontrib><creatorcontrib>Peng, Xueqi</creatorcontrib><creatorcontrib>Zhang, Xiaodong</creatorcontrib><creatorcontrib>Li, Chunyang</creatorcontrib><creatorcontrib>Gao, Chengjiang</creatorcontrib><creatorcontrib>Li, Nailin</creatorcontrib><creatorcontrib>Gao, Lifen</creatorcontrib><creatorcontrib>Liang, Xiaohong</creatorcontrib><creatorcontrib>Wu, Zhuanchang</creatorcontrib><creatorcontrib>Ma, Chunhong</creatorcontrib><title>Hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1-mediated viral RNA editing in hepatocytes</title><title>Cellular & molecular immunology</title><addtitle>Cell Mol Immunol</addtitle><addtitle>Cell Mol Immunol</addtitle><description>HBV is considered as a “stealth” virus that does not invoke interferon (IFN) responses; however, the mechanisms by which HBV bypasses innate immune recognition are poorly understood. In this study, we identified adenosine deaminases acting on RNA 1 (ADAR1), which is a key factor in HBV evasion from IFN responses in hepatocytes. Mechanically, ADAR1 interacted with HBV RNAs and deaminated adenosine (A) to generate inosine (I), which disrupted host immune recognition and thus promoted HBV replication. Loss of ADAR1 or its deficient deaminase activity promoted IFN responses and inhibited HBV replication in hepatocytes, and blocking the IFN signaling pathways released the inhibition of HBV replication caused by ADAR1 deficiency. Notably, the HBV X protein (HBx) transcriptionally promoted ADAR1 expression to increase the threshold required to trigger intrinsic immune activation, which in turn enhanced HBV escape from immune recognition, leading to persistent infection. Supplementation with 8-azaadenosine, an ADAR1 inhibitor, efficiently enhanced liver immune activation to promote HBV clearance in vivo and in vitro. Taken together, our results delineate a molecular mechanism by which HBx promotes ADAR1-derived HBV immune escape and suggest a targeted therapeutic intervention for HBV infection.</description><subject>631/250/254</subject><subject>631/250/255/234/2513/1549</subject><subject>Adenosine</subject><subject>Adenosine deaminase</subject><subject>Adenosine Deaminase - genetics</subject><subject>Adenosine Deaminase - metabolism</subject><subject>Antibodies</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Hepatitis B</subject><subject>Hepatitis B virus - metabolism</subject><subject>Hepatocytes</subject><subject>Hepatocytes - metabolism</subject><subject>Immune clearance</subject><subject>Immune response</subject><subject>Immunology</subject><subject>Interferon</subject><subject>Medical Microbiology</subject><subject>Microbiology</subject><subject>Replication</subject><subject>RNA Editing</subject><subject>RNA, Viral - genetics</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Supplements</subject><subject>Transcription</subject><subject>Vaccine</subject><issn>1672-7681</issn><issn>2042-0226</issn><issn>2042-0226</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>D8T</sourceid><recordid>eNp9kktv1DAUhS0EokPhD7BAltiwSfErtrNBGsqjSBVIFawtx7mZukzsIU6m6r_nTmdaKAsWVqx7vnucY19CXnJ2wpm0b4viSsiKCV4xZkRT8UdkIZgSWBL6MVlwbURltOVH5FkpV4zVVhn1lBxJJWpp62ZBrs9g46c4xULf020c50Jh6zsoNA7DnICOEPIqIZAT6p5efF1S1FMuEdUO_BCTL0CXH5YXvBqgi36Cbmfl17cwVqaYVjQmerk7K4ebCcpz8qT36wIvDt9j8uPTx--nZ9X5t89fTpfnVai5mCpote4a69s2CGtBG8mtwBhtsH3PTW-gabq2UVI3RuCqDZgAQspadW0vgjwm1d63XMNmbt1mjIMfb1z20R1KP3EHTmlWK438uz2PCoYJkCYM8qDtoZLipVvlrbNSCHwENHhzMBjzrxnK5IZYAqzXPkGeixM1BuNM8wbR1_-gV3keE17HjtJcNVzvKLGnwphLGaG__xnO3G4O3H4OHM6Bu50Dx7Hp1d8x7lvuHh4BebgXlNIKxj9n_8f2N1ZVv2E</recordid><startdate>20210801</startdate><enddate>20210801</enddate><creator>Wang, Liyuan</creator><creator>Sun, Yang</creator><creator>Song, Xiaojia</creator><creator>Wang, Zehua</creator><creator>Zhang, Yankun</creator><creator>Zhao, Ying</creator><creator>Peng, Xueqi</creator><creator>Zhang, Xiaodong</creator><creator>Li, Chunyang</creator><creator>Gao, Chengjiang</creator><creator>Li, Nailin</creator><creator>Gao, Lifen</creator><creator>Liang, Xiaohong</creator><creator>Wu, Zhuanchang</creator><creator>Ma, Chunhong</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope><orcidid>https://orcid.org/0000-0002-5798-2274</orcidid><orcidid>https://orcid.org/0000-0002-8121-4718</orcidid><orcidid>https://orcid.org/0000-0002-9365-4497</orcidid><orcidid>https://orcid.org/0000-0002-3848-7251</orcidid></search><sort><creationdate>20210801</creationdate><title>Hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1-mediated viral RNA editing in hepatocytes</title><author>Wang, Liyuan ; Sun, Yang ; Song, Xiaojia ; Wang, Zehua ; Zhang, Yankun ; Zhao, Ying ; Peng, Xueqi ; Zhang, Xiaodong ; Li, Chunyang ; Gao, Chengjiang ; Li, Nailin ; Gao, Lifen ; Liang, Xiaohong ; Wu, Zhuanchang ; Ma, Chunhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-eb66d98abbc288e673182058bc8ff17f7e99db943697269757e7ce23354dbf2c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>631/250/254</topic><topic>631/250/255/234/2513/1549</topic><topic>Adenosine</topic><topic>Adenosine deaminase</topic><topic>Adenosine Deaminase - genetics</topic><topic>Adenosine Deaminase - metabolism</topic><topic>Antibodies</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Hepatitis B</topic><topic>Hepatitis B virus - metabolism</topic><topic>Hepatocytes</topic><topic>Hepatocytes - metabolism</topic><topic>Immune clearance</topic><topic>Immune response</topic><topic>Immunology</topic><topic>Interferon</topic><topic>Medical Microbiology</topic><topic>Microbiology</topic><topic>Replication</topic><topic>RNA Editing</topic><topic>RNA, Viral - genetics</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Supplements</topic><topic>Transcription</topic><topic>Vaccine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Liyuan</creatorcontrib><creatorcontrib>Sun, Yang</creatorcontrib><creatorcontrib>Song, Xiaojia</creatorcontrib><creatorcontrib>Wang, Zehua</creatorcontrib><creatorcontrib>Zhang, Yankun</creatorcontrib><creatorcontrib>Zhao, Ying</creatorcontrib><creatorcontrib>Peng, Xueqi</creatorcontrib><creatorcontrib>Zhang, Xiaodong</creatorcontrib><creatorcontrib>Li, Chunyang</creatorcontrib><creatorcontrib>Gao, Chengjiang</creatorcontrib><creatorcontrib>Li, Nailin</creatorcontrib><creatorcontrib>Gao, Lifen</creatorcontrib><creatorcontrib>Liang, Xiaohong</creatorcontrib><creatorcontrib>Wu, Zhuanchang</creatorcontrib><creatorcontrib>Ma, Chunhong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><jtitle>Cellular & molecular immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Liyuan</au><au>Sun, Yang</au><au>Song, Xiaojia</au><au>Wang, Zehua</au><au>Zhang, Yankun</au><au>Zhao, Ying</au><au>Peng, Xueqi</au><au>Zhang, Xiaodong</au><au>Li, Chunyang</au><au>Gao, Chengjiang</au><au>Li, Nailin</au><au>Gao, Lifen</au><au>Liang, Xiaohong</au><au>Wu, Zhuanchang</au><au>Ma, Chunhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1-mediated viral RNA editing in hepatocytes</atitle><jtitle>Cellular & molecular immunology</jtitle><stitle>Cell Mol Immunol</stitle><addtitle>Cell Mol Immunol</addtitle><date>2021-08-01</date><risdate>2021</risdate><volume>18</volume><issue>8</issue><spage>1871</spage><epage>1882</epage><pages>1871-1882</pages><issn>1672-7681</issn><issn>2042-0226</issn><eissn>2042-0226</eissn><abstract>HBV is considered as a “stealth” virus that does not invoke interferon (IFN) responses; however, the mechanisms by which HBV bypasses innate immune recognition are poorly understood. In this study, we identified adenosine deaminases acting on RNA 1 (ADAR1), which is a key factor in HBV evasion from IFN responses in hepatocytes. Mechanically, ADAR1 interacted with HBV RNAs and deaminated adenosine (A) to generate inosine (I), which disrupted host immune recognition and thus promoted HBV replication. Loss of ADAR1 or its deficient deaminase activity promoted IFN responses and inhibited HBV replication in hepatocytes, and blocking the IFN signaling pathways released the inhibition of HBV replication caused by ADAR1 deficiency. Notably, the HBV X protein (HBx) transcriptionally promoted ADAR1 expression to increase the threshold required to trigger intrinsic immune activation, which in turn enhanced HBV escape from immune recognition, leading to persistent infection. Supplementation with 8-azaadenosine, an ADAR1 inhibitor, efficiently enhanced liver immune activation to promote HBV clearance in vivo and in vitro. Taken together, our results delineate a molecular mechanism by which HBx promotes ADAR1-derived HBV immune escape and suggest a targeted therapeutic intervention for HBV infection.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>34253859</pmid><doi>10.1038/s41423-021-00729-1</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-5798-2274</orcidid><orcidid>https://orcid.org/0000-0002-8121-4718</orcidid><orcidid>https://orcid.org/0000-0002-9365-4497</orcidid><orcidid>https://orcid.org/0000-0002-3848-7251</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1672-7681 |
| ispartof | Cellular & molecular immunology, 2021-08, Vol.18 (8), p.1871-1882 |
| issn | 1672-7681 2042-0226 2042-0226 |
| language | eng |
| recordid | cdi_swepub_primary_oai_swepub_ki_se_460546 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection; SWEPUB Freely available online |
| subjects | 631/250/254 631/250/255/234/2513/1549 Adenosine Adenosine deaminase Adenosine Deaminase - genetics Adenosine Deaminase - metabolism Antibodies Biomedical and Life Sciences Biomedicine Hepatitis B Hepatitis B virus - metabolism Hepatocytes Hepatocytes - metabolism Immune clearance Immune response Immunology Interferon Medical Microbiology Microbiology Replication RNA Editing RNA, Viral - genetics RNA-Binding Proteins - metabolism Supplements Transcription Vaccine |
| title | Hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1-mediated viral RNA editing in hepatocytes |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-04T06%3A09%3A36IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_swepu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Hepatitis%20B%20virus%20evades%20immune%20recognition%20via%20RNA%20adenosine%20deaminase%20ADAR1-mediated%20viral%20RNA%20editing%20in%20hepatocytes&rft.jtitle=Cellular%20&%20molecular%20immunology&rft.au=Wang,%20Liyuan&rft.date=2021-08-01&rft.volume=18&rft.issue=8&rft.spage=1871&rft.epage=1882&rft.pages=1871-1882&rft.issn=1672-7681&rft.eissn=2042-0226&rft_id=info:doi/10.1038/s41423-021-00729-1&rft_dat=%3Cproquest_swepu%3E2556149169%3C/proquest_swepu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2556149169&rft_id=info:pmid/34253859&rfr_iscdi=true |