Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication
Identifieur interne : 001275 ( Istex/Corpus ); précédent : 001274; suivant : 001276Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication
Auteurs : Chang-Zheng Li ; Naoya Kato ; Jin-Hai Chang ; Ryosuke Muroyama ; Run-Xuan Shao ; Narayan Dharel ; Radsamee Sermsathanasawadi ; Takao Kawabe ; Masao OmataSource :
- Liver International [ 1478-3223 ] ; 2009-10.
English descriptors
- Teeft :
- Allele, Brosis, Brosis progression, Cells harbouring, Chronic hepatitis, Cirrhosis, Clinical manifestations, Coding sequence, Core protein, Dsrna, Exon, Genome, Genotype, Harbouring, Hepatitis, Hepatocellular carcinoma, Higher degree, Huh7, Huh7 cells, Huh7 cells harbouring, Interferon, Japanese patients, John wiley sons, Liver cells, Liver cirrhosis, Liver disease, Luciferase, Luciferase activities, Minor allele, Multivariate analysis, Nucleotide, Odds ratio, Oligoadenylate, Oligoadenylate synthetase, Plasmid, Platelet count, Polymerase chain reaction, Polymorphism, Progression, Promoter, Prothrombin time, Replication, Replicon, Serum albumin level, Single nucleotide polymorphisms, Snp, Subgenomic, Subgenomic replicon, Synthetase, Transfection, Treatment response, Untranslated region, Viral, Virus infection, Virus replication.
Abstract
Background: Progression of disease after hepatitis C virus (HCV) infection differs among individuals, indicating a possibility of participation of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS‐1), an important component of the innate immune system, has an antiviral function, and may therefore have a certain relationship with progression of disease. Aim: To evaluate single nucleotide polymorphisms (SNPs) of OAS‐1 and its relationship with the disease status of HCV infection. Methods: Six SNPs of OAS‐1 were selected and examined in 409 Japanese patients with chronic HCV infection using the TaqMan PCR genotyping method. The relationship of SNP genotypes and clinical manifestations of patients was analysed. Then, a pair of OAS‐1‐expression plasmids mimicking the clinical‐related SNPs were created and transfected into liver cells carrying the HCV subgenomic replicon or the full‐length genome, JFH1, and HCV replication after transfection was compared. Results: Patients with genotypes A/A, A/G and G/G of an SNP of OAS‐1 at the exon 3 of its coding sequence were at gradient increased risks of suffering from higher serum alanine aminotransferase (P<0.001) and aspartate aminotransferase (P=0.001), higher degree of liver fibrosis (P=0.010) and higher presence of liver cirrhosis (P=0.001). By multivariate logistic regression analysis, genotype G/G was an independent factor associated with cirrhosis (P=0.013, odds ratio 3.11, 95% confidence interval 1.27–7.63). In liver cells, OAS‐1 with the G allele showed lower ability to inhibit virus replication than OAS‐1 with the A allele (P=0.004). Conclusions: The SNP of OAS‐1 at the exon 3 of its coding sequence was associated with progression of disease in Japanese patients with HCV infection.
Url:
DOI: 10.1111/j.1478-3231.2009.02061.x
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ISTEX:7A644E09A23541BF127936DBB19B7443DB6DD7A1Le document en format XML
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Kawabe</name><affiliation><mods:affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Omata, Masao" sort="Omata, Masao" uniqKey="Omata M" first="Masao" last="Omata">Masao Omata</name><affiliation><mods:affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:7A644E09A23541BF127936DBB19B7443DB6DD7A1</idno><date when="2009" year="2009">2009</date><idno type="doi">10.1111/j.1478-3231.2009.02061.x</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-3H4SMQL1-J/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001275</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001275</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication</title><author><name sortKey="Li, Chang Heng" sort="Li, Chang Heng" uniqKey="Li C" first="Chang-Zheng" last="Li">Chang-Zheng Li</name><affiliation><mods:affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Gastroenterology and Hepatology, Chinese PLA General Hospital, Beijing, China</mods:affiliation></affiliation></author><author><name sortKey="Kato, Naoya" sort="Kato, Naoya" uniqKey="Kato N" first="Naoya" last="Kato">Naoya Kato</name><affiliation><mods:affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Unit of Disease Control Genome Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Chang, Jin Ai" sort="Chang, Jin Ai" uniqKey="Chang J" first="Jin-Hai" last="Chang">Jin-Hai Chang</name><affiliation><mods:affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Muroyama, Ryosuke" sort="Muroyama, Ryosuke" uniqKey="Muroyama R" first="Ryosuke" last="Muroyama">Ryosuke Muroyama</name><affiliation><mods:affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Unit of Disease Control Genome Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Shao, Run Uan" sort="Shao, Run Uan" uniqKey="Shao R" first="Run-Xuan" last="Shao">Run-Xuan Shao</name><affiliation><mods:affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Dharel, Narayan" sort="Dharel, Narayan" uniqKey="Dharel N" first="Narayan" last="Dharel">Narayan Dharel</name><affiliation><mods:affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Sermsathanasawadi, Radsamee" sort="Sermsathanasawadi, Radsamee" uniqKey="Sermsathanasawadi R" first="Radsamee" last="Sermsathanasawadi">Radsamee Sermsathanasawadi</name><affiliation><mods:affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kawabe, Takao" sort="Kawabe, Takao" uniqKey="Kawabe T" first="Takao" last="Kawabe">Takao Kawabe</name><affiliation><mods:affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Omata, Masao" sort="Omata, Masao" uniqKey="Omata M" first="Masao" last="Omata">Masao Omata</name><affiliation><mods:affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Liver International</title><title level="j" type="alt">LIVER INTERNATIONAL</title><idno type="ISSN">1478-3223</idno><idno type="eISSN">1478-3231</idno><imprint><biblScope unit="vol">29</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1413">1413</biblScope><biblScope unit="page" to="1421">1421</biblScope><biblScope unit="page-count">9</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2009-10">2009-10</date></imprint><idno type="ISSN">1478-3223</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1478-3223</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Allele</term><term>Brosis</term><term>Brosis progression</term><term>Cells harbouring</term><term>Chronic hepatitis</term><term>Cirrhosis</term><term>Clinical manifestations</term><term>Coding sequence</term><term>Core protein</term><term>Dsrna</term><term>Exon</term><term>Genome</term><term>Genotype</term><term>Harbouring</term><term>Hepatitis</term><term>Hepatocellular carcinoma</term><term>Higher degree</term><term>Huh7</term><term>Huh7 cells</term><term>Huh7 cells harbouring</term><term>Interferon</term><term>Japanese patients</term><term>John wiley sons</term><term>Liver cells</term><term>Liver cirrhosis</term><term>Liver disease</term><term>Luciferase</term><term>Luciferase activities</term><term>Minor allele</term><term>Multivariate analysis</term><term>Nucleotide</term><term>Odds ratio</term><term>Oligoadenylate</term><term>Oligoadenylate synthetase</term><term>Plasmid</term><term>Platelet count</term><term>Polymerase chain reaction</term><term>Polymorphism</term><term>Progression</term><term>Promoter</term><term>Prothrombin time</term><term>Replication</term><term>Replicon</term><term>Serum albumin level</term><term>Single nucleotide polymorphisms</term><term>Snp</term><term>Subgenomic</term><term>Subgenomic replicon</term><term>Synthetase</term><term>Transfection</term><term>Treatment response</term><term>Untranslated region</term><term>Viral</term><term>Virus infection</term><term>Virus replication</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: Progression of disease after hepatitis C virus (HCV) infection differs among individuals, indicating a possibility of participation of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS‐1), an important component of the innate immune system, has an antiviral function, and may therefore have a certain relationship with progression of disease. Aim: To evaluate single nucleotide polymorphisms (SNPs) of OAS‐1 and its relationship with the disease status of HCV infection. Methods: Six SNPs of OAS‐1 were selected and examined in 409 Japanese patients with chronic HCV infection using the TaqMan PCR genotyping method. The relationship of SNP genotypes and clinical manifestations of patients was analysed. Then, a pair of OAS‐1‐expression plasmids mimicking the clinical‐related SNPs were created and transfected into liver cells carrying the HCV subgenomic replicon or the full‐length genome, JFH1, and HCV replication after transfection was compared. Results: Patients with genotypes A/A, A/G and G/G of an SNP of OAS‐1 at the exon 3 of its coding sequence were at gradient increased risks of suffering from higher serum alanine aminotransferase (P<0.001) and aspartate aminotransferase (P=0.001), higher degree of liver fibrosis (P=0.010) and higher presence of liver cirrhosis (P=0.001). By multivariate logistic regression analysis, genotype G/G was an independent factor associated with cirrhosis (P=0.013, odds ratio 3.11, 95% confidence interval 1.27–7.63). In liver cells, OAS‐1 with the G allele showed lower ability to inhibit virus replication than OAS‐1 with the A allele (P=0.004). Conclusions: The SNP of OAS‐1 at the exon 3 of its coding sequence was associated with progression of disease in Japanese patients with HCV infection.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>genotype</json:string><json:string>polymorphism</json:string><json:string>brosis</json:string><json:string>plasmid</json:string><json:string>allele</json:string><json:string>cirrhosis</json:string><json:string>replicon</json:string><json:string>oligoadenylate</json:string><json:string>synthetase</json:string><json:string>subgenomic</json:string><json:string>exon</json:string><json:string>transfection</json:string><json:string>viral</json:string><json:string>oligoadenylate synthetase</json:string><json:string>brosis progression</json:string><json:string>subgenomic replicon</json:string><json:string>genome</json:string><json:string>chronic hepatitis</json:string><json:string>liver disease</json:string><json:string>liver 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allele</json:string><json:string>luciferase activities</json:string><json:string>cells harbouring</json:string><json:string>platelet count</json:string><json:string>untranslated region</json:string><json:string>multivariate analysis</json:string><json:string>huh7 cells harbouring</json:string><json:string>single nucleotide polymorphisms</json:string><json:string>japanese patients</json:string><json:string>polymerase chain reaction</json:string><json:string>nucleotide</json:string></teeft></keywords><author><json:item><name>Chang‐Zheng Li</name><affiliations><json:string>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</json:string><json:string>Department of Gastroenterology and Hepatology, Chinese PLA General Hospital, Beijing, China</json:string></affiliations></json:item><json:item><name>Naoya Kato</name><affiliations><json:string>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</json:string><json:string>Unit of Disease Control Genome Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Jin‐Hai Chang</name><affiliations><json:string>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Ryosuke Muroyama</name><affiliations><json:string>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</json:string><json:string>Unit of Disease Control Genome Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Run‐Xuan Shao</name><affiliations><json:string>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Narayan Dharel</name><affiliations><json:string>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Radsamee Sermsathanasawadi</name><affiliations><json:string>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Takao Kawabe</name><affiliations><json:string>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Masao Omata</name><affiliations><json:string>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>cirrhosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>fibrosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>JFH1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>replicon</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SNP</value></json:item></subject><articleId><json:string>LIV2061</json:string></articleId><arkIstex>ark:/67375/WNG-3H4SMQL1-J</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Background: Progression of disease after hepatitis C virus (HCV) infection differs among individuals, indicating a possibility of participation of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS‐1), an important component of the innate immune system, has an antiviral function, and may therefore have a certain relationship with progression of disease. Aim: To evaluate single nucleotide polymorphisms (SNPs) of OAS‐1 and its relationship with the disease status of HCV infection. Methods: Six SNPs of OAS‐1 were selected and examined in 409 Japanese patients with chronic HCV infection using the TaqMan PCR genotyping method. The relationship of SNP genotypes and clinical manifestations of patients was analysed. Then, a pair of OAS‐1‐expression plasmids mimicking the clinical‐related SNPs were created and transfected into liver cells carrying the HCV subgenomic replicon or the full‐length genome, JFH1, and HCV replication after transfection was compared. Results: Patients with genotypes A/A, A/G and G/G of an SNP of OAS‐1 at the exon 3 of its coding sequence were at gradient increased risks of suffering from higher serum alanine aminotransferase (P>0.001) and aspartate aminotransferase (P=0.001), higher degree of liver fibrosis (P=0.010) and higher presence of liver cirrhosis (P=0.001). By multivariate logistic regression analysis, genotype G/G was an independent factor associated with cirrhosis (P=0.013, odds ratio 3.11, 95% confidence interval 1.27–7.63). In liver cells, OAS‐1 with the G allele showed lower ability to inhibit virus replication than OAS‐1 with the A allele (P=0.004). Conclusions: The SNP of OAS‐1 at the exon 3 of its coding sequence was associated with progression of disease in Japanese patients with HCV infection.</abstract><qualityIndicators><score>10</score><pdfWordCount>5494</pdfWordCount><pdfCharCount>35277</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>612.283 x 799.37 pts</pdfPageSize><pdfWordsPerPage>610</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>257</abstractWordCount><abstractCharCount>1768</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication</title><pmid><json:string>19515215</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Liver International</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1478-3231</json:string></doi><issn><json:string>1478-3223</json:string></issn><eissn><json:string>1478-3231</json:string></eissn><publisherId><json:string>LIV</json:string></publisherId><volume>29</volume><issue>9</issue><pages><first>1413</first><last>1421</last><total>9</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2009</json:string><json:string>between August 2001 and June 2003</json:string><json:string>4-6-1</json:string></date><geogName></geogName><orgName><json:string>SPSS Inc., Chicago</json:string><json:string>Institute of Medical Science, University of Tokyo, Tokyo, Japan Keywords</json:string><json:string>Ortho Diagnostics, Tokyo, Japan</json:string><json:string>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</json:string><json:string>University of Tokyo Hospital</json:string><json:string>General Hospital, Beijing, China</json:string><json:string>Institute of Medical Science, University of Tokyo</json:string><json:string>Japan Tel</json:string><json:string>Ministry of Education, Culture, Sports, Science and Technology of Japan</json:string><json:string>Ministry of Health, Labor and Welfare, Japan</json:string><json:string>Labor Sciences Research Grants for Research on Hepatitis</json:string><json:string>Department of Gastroenterology and Hepatology</json:string><json:string>Bio-Rad Laboratories</json:string><json:string>Education and Research for Advanced Genome-Based Medicine</json:string><json:string>Abbott Laboratories</json:string><json:string>Liver International</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Xuan Shao</json:string><json:string>John Wiley</json:string><json:string>Knapp</json:string><json:string>Naoya Kato</json:string><json:string>C. Acknowledgements</json:string><json:string>Jin-Hai Chang</json:string><json:string>Narayan Dharel</json:string></persName><placeName><json:string>TX</json:string><json:string>Bad Wildbad</json:string><json:string>Nile</json:string><json:string>Leiden</json:string><json:string>Foster City</json:string><json:string>Germany</json:string><json:string>Austin</json:string><json:string>USA</json:string><json:string>Japan</json:string><json:string>Tokyo</json:string><json:string>Chicago</json:string><json:string>CA</json:string><json:string>Hercules</json:string></placeName><ref_url><json:string>http://snp.ims.u-tokyo.ac.jp</json:string><json:string>ftp://linkage.rocke</json:string></ref_url><ref_bibl><json:string>Ghany et al.</json:string><json:string>Li et al.</json:string><json:string>Knapp et al.</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-3H4SMQL1-J</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - 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C</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><licence>© 2009 John Wiley & Sons A/S</licence></availability><date type="published" when="2009-10"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication</title><title level="a" type="short">Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C</title><author xml:id="author-0000"><persName><forename type="first">Chang‐Zheng</forename><surname>Li</surname></persName><affiliation><orgName type="department">Department of Gastroenterology</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">University of Tokyo</orgName><address><addrLine>Tokyo</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation><affiliation><orgName type="department">Department of Gastroenterology and Hepatology</orgName><orgName type="institution">Chinese PLA General Hospital</orgName><address><addrLine>Beijing</addrLine><addrLine>China</addrLine><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Naoya</forename><surname>Kato</surname></persName><affiliation><orgName type="department">Department of Gastroenterology</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">University of Tokyo</orgName><address><addrLine>Tokyo</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation><affiliation><orgName type="laboratory">Unit of Disease Control Genome Medicine</orgName><orgName type="institution">Institute of Medical Science</orgName><orgName type="institution">University of Tokyo</orgName><address><addrLine>Tokyo</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Jin‐Hai</forename><surname>Chang</surname></persName><affiliation><orgName type="department">Department of Gastroenterology</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">University of Tokyo</orgName><address><addrLine>Tokyo</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Ryosuke</forename><surname>Muroyama</surname></persName><affiliation><orgName type="department">Department of Gastroenterology</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">University of Tokyo</orgName><address><addrLine>Tokyo</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation><affiliation><orgName type="laboratory">Unit of Disease Control Genome Medicine</orgName><orgName type="institution">Institute of Medical Science</orgName><orgName type="institution">University of Tokyo</orgName><address><addrLine>Tokyo</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Run‐Xuan</forename><surname>Shao</surname></persName><affiliation><orgName type="department">Department of Gastroenterology</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">University of Tokyo</orgName><address><addrLine>Tokyo</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Narayan</forename><surname>Dharel</surname></persName><affiliation><orgName type="department">Department of Gastroenterology</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">University of Tokyo</orgName><address><addrLine>Tokyo</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Radsamee</forename><surname>Sermsathanasawadi</surname></persName><affiliation><orgName type="department">Department of Gastroenterology</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">University of Tokyo</orgName><address><addrLine>Tokyo</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">Takao</forename><surname>Kawabe</surname></persName><affiliation><orgName type="department">Department of Gastroenterology</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">University of Tokyo</orgName><address><addrLine>Tokyo</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><author xml:id="author-0008"><persName><forename type="first">Masao</forename><surname>Omata</surname></persName><affiliation><orgName type="department">Department of Gastroenterology</orgName><orgName type="department">Graduate School of Medicine</orgName><orgName type="institution">University of Tokyo</orgName><address><addrLine>Tokyo</addrLine><addrLine>Japan</addrLine><country key="JP" xml:lang="en">JAPAN</country></address></affiliation></author><idno type="istex">7A644E09A23541BF127936DBB19B7443DB6DD7A1</idno><idno type="ark">ark:/67375/WNG-3H4SMQL1-J</idno><idno type="DOI">10.1111/j.1478-3231.2009.02061.x</idno><idno type="unit">LIV2061</idno><idno type="supplier">2061</idno><idno type="toTypesetVersion">file:LIV.LIV2061.pdf</idno></analytic><monogr><title level="j" type="main">Liver International</title><title level="j" type="alt">LIVER INTERNATIONAL</title><idno type="pISSN">1478-3223</idno><idno type="eISSN">1478-3231</idno><idno type="book-DOI">10.1111/(ISSN)1478-3231</idno><idno type="book-part-DOI">10.1111/liv.2009.29.issue-9</idno><idno type="product">LIV</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">29</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1413">1413</biblScope><biblScope unit="page" to="1421">1421</biblScope><biblScope unit="page-count">9</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2009-10"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><encodingDesc><schemaRef type="ODD" url="https://xml-schema.delivery.istex.fr/tei-istex.odd"></schemaRef><appInfo><application ident="pub2tei" version="1.0.10" when="2019-12-20"><label>pub2TEI-ISTEX</label><desc>A set of style sheets for converting XML documents encoded in various scientific publisher formats into a common TEI format.
<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p><hi rend="bold">Background: </hi> Progression of disease after hepatitis C virus (HCV) infection differs among individuals, indicating a possibility of participation of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS‐1), an important component of the innate immune system, has an antiviral function, and may therefore have a certain relationship with progression of disease.</p><p><hi rend="bold">Aim: </hi> To evaluate single nucleotide polymorphisms (SNPs) of OAS‐1 and its relationship with the disease status of HCV infection.</p><p><hi rend="bold">Methods: </hi> Six SNPs of OAS‐1 were selected and examined in 409 Japanese patients with chronic HCV infection using the TaqMan PCR genotyping method. The relationship of SNP genotypes and clinical manifestations of patients was analysed. Then, a pair of OAS‐1‐expression plasmids mimicking the clinical‐related SNPs were created and transfected into liver cells carrying the HCV subgenomic replicon or the full‐length genome, JFH1, and HCV replication after transfection was compared.</p><p><hi rend="bold">Results: </hi> Patients with genotypes A/A, A/G and G/G of an SNP of OAS‐1 at the exon 3 of its coding sequence were at gradient increased risks of suffering from higher serum alanine aminotransferase (<hi rend="italic">P</hi><0.001) and aspartate aminotransferase (<hi rend="italic">P</hi>=0.001), higher degree of liver fibrosis (<hi rend="italic">P</hi>=0.010) and higher presence of liver cirrhosis (<hi rend="italic">P</hi>=0.001). By multivariate logistic regression analysis, genotype G/G was an independent factor associated with cirrhosis (<hi rend="italic">P</hi>=0.013, odds ratio 3.11, 95% confidence interval 1.27–7.63). In liver cells, OAS‐1 with the G allele showed lower ability to inhibit virus replication than OAS‐1 with the A allele (<hi rend="italic">P</hi>=0.004).</p><p><hi rend="bold">Conclusions: </hi> The SNP of OAS‐1 at the exon 3 of its coding sequence was associated with progression of disease in Japanese patients with HCV infection.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">cirrhosis</term><term xml:id="k2">fibrosis</term><term xml:id="k3">JFH1</term><term xml:id="k4">replicon</term><term xml:id="k5">SNP</term></keywords><keywords rend="tocHeading1"><term>Clinical Studies</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-3H4SMQL1-J/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1478-3231</doi><issn type="print">1478-3223</issn><issn type="electronic">1478-3231</issn><idGroup><id type="product" value="LIV"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="LIVER INTERNATIONAL">Liver International</title></titleGroup></publicationMeta><publicationMeta level="part" position="10009"><doi origin="wiley">10.1111/liv.2009.29.issue-9</doi><numberingGroup><numbering type="journalVolume" number="29">29</numbering><numbering type="journalIssue" number="9">9</numbering></numberingGroup><coverDate startDate="2009-10">October 2009</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="16" status="forIssue"><doi origin="wiley">10.1111/j.1478-3231.2009.02061.x</doi><idGroup><id type="unit" value="LIV2061"></id><id type="supplier" value="2061"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="tocHeading1">Clinical Studies</title></titleGroup><copyright>© 2009 John Wiley & Sons A/S</copyright><eventGroup><event type="firstOnline" date="2009-06-09"></event><event type="publishedOnlineFinalForm" date="2009-09-03"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.4 mode:FullText source:FullText result:FullText" date="2010-03-30"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-01"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="1413">1413</numbering><numbering type="pageLast" number="1421">1421</numbering></numberingGroup><correspondenceTo><b>Correspondence</b>
Naoya Kato, MD, Unit of Disease Control Genome Medicine, Institute of Medical Science, University of Tokyo, 4‐6‐1 Shirokanedai, Minato‐ku, Tokyo 108‐8639, Japan
Tel: +81‐3‐6409‐2335
Fax: +81‐3‐6409‐2336
e‐mail: <email normalForm="kato-2im@ims.u-tokyo.ac.jp">kato‐2im@ims.u‐tokyo.ac.jp</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:LIV.LIV2061.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 29 March 2009Accepted 5 May 2009</unparsedEditorialHistory><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="8"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="40"></count><count type="wordTotal" number="7410"></count><count type="linksCrossRef" number="58"></count></countGroup><titleGroup><title type="main">Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication</title><title type="shortAuthors">Li <i>et al.</i></title><title type="short">Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>Chang‐Zheng</givenNames><familyName>Li</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1 #a3"><personName><givenNames>Naoya</givenNames><familyName>Kato</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Jin‐Hai</givenNames><familyName>Chang</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1 #a3"><personName><givenNames>Ryosuke</givenNames><familyName>Muroyama</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Run‐Xuan</givenNames><familyName>Shao</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>Narayan</givenNames><familyName>Dharel</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>Radsamee</givenNames><familyName>Sermsathanasawadi</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a1"><personName><givenNames>Takao</givenNames><familyName>Kawabe</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a1"><personName><givenNames>Masao</givenNames><familyName>Omata</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="JP"><unparsedAffiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="CN"><unparsedAffiliation>Department of Gastroenterology and Hepatology, Chinese PLA General Hospital, Beijing, China</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="JP"><unparsedAffiliation>Unit of Disease Control Genome Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">cirrhosis</keyword><keyword xml:id="k2">fibrosis</keyword><keyword xml:id="k3">JFH1</keyword><keyword xml:id="k4">replicon</keyword><keyword xml:id="k5">SNP</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p><b>Background: </b> Progression of disease after hepatitis C virus (HCV) infection differs among individuals, indicating a possibility of participation of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS‐1), an important component of the innate immune system, has an antiviral function, and may therefore have a certain relationship with progression of disease.</p><p><b>Aim: </b> To evaluate single nucleotide polymorphisms (SNPs) of OAS‐1 and its relationship with the disease status of HCV infection.</p><p><b>Methods: </b> Six SNPs of OAS‐1 were selected and examined in 409 Japanese patients with chronic HCV infection using the TaqMan PCR genotyping method. The relationship of SNP genotypes and clinical manifestations of patients was analysed. Then, a pair of OAS‐1‐expression plasmids mimicking the clinical‐related SNPs were created and transfected into liver cells carrying the HCV subgenomic replicon or the full‐length genome, JFH1, and HCV replication after transfection was compared.</p><p><b>Results: </b> Patients with genotypes A/A, A/G and G/G of an SNP of OAS‐1 at the exon 3 of its coding sequence were at gradient increased risks of suffering from higher serum alanine aminotransferase (<i>P</i><0.001) and aspartate aminotransferase (<i>P</i>=0.001), higher degree of liver fibrosis (<i>P</i>=0.010) and higher presence of liver cirrhosis (<i>P</i>=0.001). By multivariate logistic regression analysis, genotype G/G was an independent factor associated with cirrhosis (<i>P</i>=0.013, odds ratio 3.11, 95% confidence interval 1.27–7.63). In liver cells, OAS‐1 with the G allele showed lower ability to inhibit virus replication than OAS‐1 with the A allele (<i>P</i>=0.004).</p><p><b>Conclusions: </b> The SNP of OAS‐1 at the exon 3 of its coding sequence was associated with progression of disease in Japanese patients with HCV infection.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Polymorphism of OAS‐1 determines liver fibrosis progression in hepatitis C by reduced ability to inhibit viral replication</title></titleInfo><name type="personal"><namePart type="given">Chang‐Zheng</namePart><namePart type="family">Li</namePart><affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</affiliation><affiliation>Department of Gastroenterology and Hepatology, Chinese PLA General Hospital, Beijing, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Naoya</namePart><namePart type="family">Kato</namePart><affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</affiliation><affiliation>Unit of Disease Control Genome Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jin‐Hai</namePart><namePart type="family">Chang</namePart><affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ryosuke</namePart><namePart type="family">Muroyama</namePart><affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</affiliation><affiliation>Unit of Disease Control Genome Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Run‐Xuan</namePart><namePart type="family">Shao</namePart><affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Narayan</namePart><namePart type="family">Dharel</namePart><affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Radsamee</namePart><namePart type="family">Sermsathanasawadi</namePart><affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takao</namePart><namePart type="family">Kawabe</namePart><affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Masao</namePart><namePart type="family">Omata</namePart><affiliation>Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2009-10</dateIssued><edition>Received 29 March 2009Accepted 5 May 2009</edition><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">3</extent><extent unit="tables">8</extent><extent unit="formulas">0</extent><extent unit="references">40</extent><extent unit="linksCrossRef">58</extent><extent unit="words">7410</extent></physicalDescription><abstract lang="en">Background: Progression of disease after hepatitis C virus (HCV) infection differs among individuals, indicating a possibility of participation of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS‐1), an important component of the innate immune system, has an antiviral function, and may therefore have a certain relationship with progression of disease. Aim: To evaluate single nucleotide polymorphisms (SNPs) of OAS‐1 and its relationship with the disease status of HCV infection. Methods: Six SNPs of OAS‐1 were selected and examined in 409 Japanese patients with chronic HCV infection using the TaqMan PCR genotyping method. The relationship of SNP genotypes and clinical manifestations of patients was analysed. Then, a pair of OAS‐1‐expression plasmids mimicking the clinical‐related SNPs were created and transfected into liver cells carrying the HCV subgenomic replicon or the full‐length genome, JFH1, and HCV replication after transfection was compared. Results: Patients with genotypes A/A, A/G and G/G of an SNP of OAS‐1 at the exon 3 of its coding sequence were at gradient increased risks of suffering from higher serum alanine aminotransferase (P<0.001) and aspartate aminotransferase (P=0.001), higher degree of liver fibrosis (P=0.010) and higher presence of liver cirrhosis (P=0.001). By multivariate logistic regression analysis, genotype G/G was an independent factor associated with cirrhosis (P=0.013, odds ratio 3.11, 95% confidence interval 1.27–7.63). In liver cells, OAS‐1 with the G allele showed lower ability to inhibit virus replication than OAS‐1 with the A allele (P=0.004). Conclusions: The SNP of OAS‐1 at the exon 3 of its coding sequence was associated with progression of disease in Japanese patients with HCV infection.</abstract><subject lang="en"><genre>keywords</genre><topic>cirrhosis</topic><topic>fibrosis</topic><topic>JFH1</topic><topic>replicon</topic><topic>SNP</topic></subject><relatedItem type="host"><titleInfo><title>Liver International</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">1478-3223</identifier><identifier type="eISSN">1478-3231</identifier><identifier type="DOI">10.1111/(ISSN)1478-3231</identifier><identifier type="PublisherID">LIV</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>29</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1413</start><end>1421</end><total>9</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>Acute hepatitis C</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Heller</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Rehermann</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Heller T, Rehermann B. Acute hepatitis C: a multifaceted disease. 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