Single nucleotide polymorphism at exon 7 splice acceptor site of OAS1 gene determines response of hepatitis C virus patients to interferon therapy
Identifieur interne : 001289 ( Istex/Corpus ); précédent : 001288; suivant : 001290Single nucleotide polymorphism at exon 7 splice acceptor site of OAS1 gene determines response of hepatitis C virus patients to interferon therapy
Auteurs : Mostafa K. El Awady ; Mohamed A. Anany ; Gamal Esmat ; Naglaa Zayed ; Ashraf A. Tabll ; Amr Helmy ; Abdel Rahman El Zayady ; Mohga S. Abdalla ; Hayat M. Sharada ; Maissa El Raziky ; Wafaa El Akel ; Shadia Abdalla ; Noha G. Bader El DinSource :
- Journal of Gastroenterology and Hepatology [ 0815-9319 ] ; 2011-05.
Abstract
Background and Aim: Response to interferon therapy and disease progression in hepatitis C virus (HCV) infected patients differs among individuals, suggesting a possibility of a contribution of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS1), an important component of the innate immune system with a proven antiviral function, may therefore have a relationship with the response to interferon therapy and clinical course of HCV disease. Our aim was to determine the frequency of single nucleotide polymorphism (SNP) at exon 7 splice acceptor site (SAS) of the OAS1 gene in relation to the interferon response and status of HCV infection. Methods: A 203 bp fragment containing exon 7 SAS was amplified in 70 HCV chronic patients and 50 healthy controls. SNP was examined using restriction fragment length polymorphism (RFLP) genotyping method. Correlations of SNP genotypes with response to interferon and clinical status of patients were statistically analyzed. Results: There was an increasing trend of response from AA to AG to GG genotypes (P = 0.007). Genotype AA was associated with non‐response to interferon and higher degree of liver fibrosis (P = 0.05). Multivariate analysis showed this SNP as independent and a significant determinant of the outcome of interferon therapy (odds ratio 4.913 [95% confidence interval 1.365–8.2], P = 0.006). Conclusions: This is the first study to show a significant association between the functional SNP at exon 7 SAS of OAS1 gene and the viral response to interferon in chronic HCV patients. Patients with AA genotype were associated with progressive HCV disease and viral resistance to interferon therapy. This OAS SNP is a potential bio‐marker to predict IFN response in chronic hepatitis C patients.
Url:
DOI: 10.1111/j.1440-1746.2010.06605.x
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Anany</name><affiliation><mods:affiliation>Department of Microbial Biotechnology, National Research Center, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Esmat, Gamal" sort="Esmat, Gamal" uniqKey="Esmat G" first="Gamal" last="Esmat">Gamal Esmat</name><affiliation><mods:affiliation>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Zayed, Naglaa" sort="Zayed, Naglaa" uniqKey="Zayed N" first="Naglaa" last="Zayed">Naglaa Zayed</name><affiliation><mods:affiliation>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Tabll, Ashraf A" sort="Tabll, Ashraf A" uniqKey="Tabll A" first="Ashraf A" last="Tabll">Ashraf A. 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El Awady</name><affiliation><mods:affiliation>Department of Microbial Biotechnology, National Research Center, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Anany, Mohamed A" sort="Anany, Mohamed A" uniqKey="Anany M" first="Mohamed A" last="Anany">Mohamed A. Anany</name><affiliation><mods:affiliation>Department of Microbial Biotechnology, National Research Center, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Esmat, Gamal" sort="Esmat, Gamal" uniqKey="Esmat G" first="Gamal" last="Esmat">Gamal Esmat</name><affiliation><mods:affiliation>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Zayed, Naglaa" sort="Zayed, Naglaa" uniqKey="Zayed N" first="Naglaa" last="Zayed">Naglaa Zayed</name><affiliation><mods:affiliation>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Tabll, Ashraf A" sort="Tabll, Ashraf A" uniqKey="Tabll A" first="Ashraf A" last="Tabll">Ashraf A. Tabll</name><affiliation><mods:affiliation>Department of Microbial Biotechnology, National Research Center, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Helmy, Amr" sort="Helmy, Amr" uniqKey="Helmy A" first="Amr" last="Helmy">Amr Helmy</name><affiliation><mods:affiliation>National Liver Institute, Shebeen El Kom, EL Monufea, Egypt</mods:affiliation></affiliation></author><author><name sortKey="El Zayady, Abdel Rahman" sort="El Zayady, Abdel Rahman" uniqKey="El Zayady A" first="Abdel Rahman" last="El Zayady">Abdel Rahman El Zayady</name><affiliation><mods:affiliation>Cairo Liver Center, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Abdalla, Mohga S" sort="Abdalla, Mohga S" uniqKey="Abdalla M" first="Mohga S" last="Abdalla">Mohga S. Abdalla</name><affiliation><mods:affiliation>Faculty of Sciences Helwan University, Helwan, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Sharada, Hayat M" sort="Sharada, Hayat M" uniqKey="Sharada H" first="Hayat M" last="Sharada">Hayat M. Sharada</name><affiliation><mods:affiliation>Faculty of Sciences Helwan University, Helwan, Egypt</mods:affiliation></affiliation></author><author><name sortKey="El Raziky, Maissa" sort="El Raziky, Maissa" uniqKey="El Raziky M" first="Maissa" last="El Raziky">Maissa El Raziky</name><affiliation><mods:affiliation>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</mods:affiliation></affiliation></author><author><name sortKey="El Akel, Wafaa" sort="El Akel, Wafaa" uniqKey="El Akel W" first="Wafaa" last="El Akel">Wafaa El Akel</name><affiliation><mods:affiliation>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Abdalla, Shadia" sort="Abdalla, Shadia" uniqKey="Abdalla S" first="Shadia" last="Abdalla">Shadia Abdalla</name><affiliation><mods:affiliation>Department of Clinical Pathology, El Sahel Teaching Hospital, Cairo, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Bader El Din, Noha G" sort="Bader El Din, Noha G" uniqKey="Bader El Din N" first="Noha G" last="Bader El Din">Noha G. Bader El Din</name><affiliation><mods:affiliation>Department of Microbial Biotechnology, National Research Center, Egypt</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: nbadereldin@yahoo.com</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Gastroenterology and Hepatology</title><title level="j" type="alt">JOURNAL OF GASTROENTEROLOGY HEPATOLOGY</title><idno type="ISSN">0815-9319</idno><idno type="eISSN">1440-1746</idno><imprint><biblScope unit="vol">26</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="843">843</biblScope><biblScope unit="page" to="850">850</biblScope><biblScope unit="page-count">8</biblScope><publisher>Blackwell Publishing Asia</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2011-05">2011-05</date></imprint><idno type="ISSN">0815-9319</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0815-9319</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background and Aim: Response to interferon therapy and disease progression in hepatitis C virus (HCV) infected patients differs among individuals, suggesting a possibility of a contribution of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS1), an important component of the innate immune system with a proven antiviral function, may therefore have a relationship with the response to interferon therapy and clinical course of HCV disease. Our aim was to determine the frequency of single nucleotide polymorphism (SNP) at exon 7 splice acceptor site (SAS) of the OAS1 gene in relation to the interferon response and status of HCV infection. Methods: A 203 bp fragment containing exon 7 SAS was amplified in 70 HCV chronic patients and 50 healthy controls. SNP was examined using restriction fragment length polymorphism (RFLP) genotyping method. Correlations of SNP genotypes with response to interferon and clinical status of patients were statistically analyzed. Results: There was an increasing trend of response from AA to AG to GG genotypes (P = 0.007). Genotype AA was associated with non‐response to interferon and higher degree of liver fibrosis (P = 0.05). Multivariate analysis showed this SNP as independent and a significant determinant of the outcome of interferon therapy (odds ratio 4.913 [95% confidence interval 1.365–8.2], P = 0.006). Conclusions: This is the first study to show a significant association between the functional SNP at exon 7 SAS of OAS1 gene and the viral response to interferon in chronic HCV patients. Patients with AA genotype were associated with progressive HCV disease and viral resistance to interferon therapy. This OAS SNP is a potential bio‐marker to predict IFN response in chronic hepatitis C patients.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>oas1</json:string><json:string>genotype</json:string><json:string>interferon</json:string><json:string>exon</json:string><json:string>allele</json:string><json:string>viral</json:string><json:string>polymorphism</json:string><json:string>hepatology</json:string><json:string>gastroenterology</json:string><json:string>synthetase</json:string><json:string>chronic hepatitis</json:string><json:string>oas1 gene</json:string><json:string>acceptor</json:string><json:string>ribavirin</json:string><json:string>antiviral</json:string><json:string>awady</json:string><json:string>interferon therapy</json:string><json:string>responder</json:string><json:string>hepatitis</json:string><json:string>liver fibrosis</json:string><json:string>virological</json:string><json:string>alui</json:string><json:string>blackwell 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bioer technology</json:string><json:string>human oas1 gene</json:string><json:string>national research center</json:string><json:string>statistical analysis</json:string><json:string>different oas1 genotype</json:string><json:string>higher degree</json:string><json:string>genetic variation</json:string><json:string>present study</json:string><json:string>interferon treatment</json:string><json:string>persistent infection</json:string><json:string>japanese patient</json:string><json:string>progression</json:string><json:string>gene</json:string></teeft></keywords><author><json:item><name>Mostafa K El Awady</name><affiliations><json:string>Department of Microbial Biotechnology, National Research Center, Egypt</json:string></affiliations></json:item><json:item><name>Mohamed A Anany</name><affiliations><json:string>Department of Microbial Biotechnology, National Research Center, Egypt</json:string></affiliations></json:item><json:item><name>Gamal Esmat</name><affiliations><json:string>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</json:string></affiliations></json:item><json:item><name>Naglaa Zayed</name><affiliations><json:string>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</json:string></affiliations></json:item><json:item><name>Ashraf A Tabll</name><affiliations><json:string>Department of Microbial Biotechnology, National Research Center, Egypt</json:string></affiliations></json:item><json:item><name>Amr Helmy</name><affiliations><json:string>National Liver Institute, Shebeen El Kom, EL Monufea, Egypt</json:string></affiliations></json:item><json:item><name>Abdel Rahman El Zayady</name><affiliations><json:string>Cairo Liver Center, Egypt</json:string></affiliations></json:item><json:item><name>Mohga S Abdalla</name><affiliations><json:string>Faculty of Sciences Helwan University, Helwan, Egypt</json:string></affiliations></json:item><json:item><name>Hayat M Sharada</name><affiliations><json:string>Faculty of Sciences Helwan University, Helwan, Egypt</json:string></affiliations></json:item><json:item><name>Maissa El Raziky</name><affiliations><json:string>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</json:string></affiliations></json:item><json:item><name>Wafaa El Akel</name><affiliations><json:string>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</json:string></affiliations></json:item><json:item><name>Shadia Abdalla</name><affiliations><json:string>Department of Clinical Pathology, El Sahel Teaching Hospital, Cairo, Egypt</json:string></affiliations></json:item><json:item><name>Noha G Bader El Din</name><affiliations><json:string>Department of Microbial Biotechnology, National Research Center, Egypt</json:string><json:string>E-mail: nbadereldin@yahoo.com</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Hepatitis C virus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>liver fibrosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>OAS1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>response to interferon therapy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>single nucleotide polymorphism</value></json:item></subject><articleId><json:string>JGH6605</json:string></articleId><arkIstex>ark:/67375/WNG-NQ0KCM1W-6</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Background and Aim: Response to interferon therapy and disease progression in hepatitis C virus (HCV) infected patients differs among individuals, suggesting a possibility of a contribution of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS1), an important component of the innate immune system with a proven antiviral function, may therefore have a relationship with the response to interferon therapy and clinical course of HCV disease. Our aim was to determine the frequency of single nucleotide polymorphism (SNP) at exon 7 splice acceptor site (SAS) of the OAS1 gene in relation to the interferon response and status of HCV infection. Methods: A 203 bp fragment containing exon 7 SAS was amplified in 70 HCV chronic patients and 50 healthy controls. SNP was examined using restriction fragment length polymorphism (RFLP) genotyping method. Correlations of SNP genotypes with response to interferon and clinical status of patients were statistically analyzed. Results: There was an increasing trend of response from AA to AG to GG genotypes (P = 0.007). Genotype AA was associated with non‐response to interferon and higher degree of liver fibrosis (P = 0.05). Multivariate analysis showed this SNP as independent and a significant determinant of the outcome of interferon therapy (odds ratio 4.913 [95% confidence interval 1.365–8.2], P = 0.006). Conclusions: This is the first study to show a significant association between the functional SNP at exon 7 SAS of OAS1 gene and the viral response to interferon in chronic HCV patients. Patients with AA genotype were associated with progressive HCV disease and viral resistance to interferon therapy. This OAS SNP is a potential bio‐marker to predict IFN response in chronic hepatitis C patients.</abstract><qualityIndicators><score>10</score><pdfWordCount>5763</pdfWordCount><pdfCharCount>35228</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>8</pdfPageCount><pdfPageSize>595.276 x 810.709 pts</pdfPageSize><pdfWordsPerPage>720</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>264</abstractWordCount><abstractCharCount>1766</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Single nucleotide polymorphism at exon 7 splice acceptor site of OAS1 gene determines response of hepatitis C virus patients to interferon therapy</title><pmid><json:string>21182542</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Gastroenterology and 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xml:id="author-0000"><persName><forename type="first">Mostafa K</forename><surname>El Awady</surname></persName><affiliation><orgName type="department">Department of Microbial Biotechnology</orgName><orgName type="institution">National Research Center</orgName><address><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Mohamed A</forename><surname>Anany</surname></persName><affiliation><orgName type="department">Department of Microbial Biotechnology</orgName><orgName type="institution">National Research Center</orgName><address><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Gamal</forename><surname>Esmat</surname></persName><affiliation><orgName type="division">Department of Tropical Medicine Gastroenterology and Liver Diseases</orgName><address><addrLine>Kasr El Aini</addrLine><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Naglaa</forename><surname>Zayed</surname></persName><affiliation><orgName type="division">Department of Tropical Medicine Gastroenterology and Liver Diseases</orgName><address><addrLine>Kasr El Aini</addrLine><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Ashraf A</forename><surname>Tabll</surname></persName><affiliation><orgName type="department">Department of Microbial Biotechnology</orgName><orgName type="institution">National Research Center</orgName><address><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Amr</forename><surname>Helmy</surname></persName><affiliation><orgName type="institution">National Liver Institute</orgName><address><addrLine>Shebeen El Kom</addrLine><addrLine>EL Monufea, Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Abdel Rahman</forename><surname>El Zayady</surname></persName><affiliation><orgName type="institution">Cairo Liver Center</orgName><address><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">Mohga S</forename><surname>Abdalla</surname></persName><affiliation><orgName type="institution">Faculty of Sciences Helwan University</orgName><address><addrLine>Helwan</addrLine><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0008"><persName><forename type="first">Hayat M</forename><surname>Sharada</surname></persName><affiliation><orgName type="institution">Faculty of Sciences Helwan University</orgName><address><addrLine>Helwan</addrLine><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0009"><persName><forename type="first">Maissa</forename><surname>El Raziky</surname></persName><affiliation><orgName type="division">Department of Tropical Medicine Gastroenterology and Liver Diseases</orgName><address><addrLine>Kasr El Aini</addrLine><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0010"><persName><forename type="first">Wafaa</forename><surname>El Akel</surname></persName><affiliation><orgName type="division">Department of Tropical Medicine Gastroenterology and Liver Diseases</orgName><address><addrLine>Kasr El Aini</addrLine><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0011"><persName><forename type="first">Shadia</forename><surname>Abdalla</surname></persName><affiliation><orgName type="department">Department of Clinical Pathology</orgName><orgName type="institution">El Sahel Teaching Hospital</orgName><address><addrLine>Cairo</addrLine><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><author xml:id="author-0012" role="corresp"><persName><forename type="first">Noha G</forename><surname>Bader El Din</surname></persName><affiliation><orgName type="department">Department of Microbial Biotechnology</orgName><orgName type="institution">National Research Center</orgName><address><addrLine>Egypt</addrLine><country key="EG" xml:lang="en">EGYPT</country></address></affiliation></author><idno type="istex">457CB480733E44162785A337F8EADA499795C331</idno><idno type="ark">ark:/67375/WNG-NQ0KCM1W-6</idno><idno type="DOI">10.1111/j.1440-1746.2010.06605.x</idno><idno type="unit">JGH6605</idno><idno type="toTypesetVersion">file:JGH.JGH6605.pdf</idno></analytic><monogr><title level="j" type="main">Journal of Gastroenterology and Hepatology</title><title level="j" type="alt">JOURNAL OF GASTROENTEROLOGY HEPATOLOGY</title><idno type="pISSN">0815-9319</idno><idno type="eISSN">1440-1746</idno><idno type="book-DOI">10.1111/(ISSN)1440-1746</idno><idno type="book-part-DOI">10.1111/jgh.2011.26.issue-5</idno><idno type="product">JGH</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">26</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="843">843</biblScope><biblScope unit="page" to="850">850</biblScope><biblScope unit="page-count">8</biblScope><publisher>Blackwell Publishing Asia</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2011-05"></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 and Aim: </hi> Response to interferon therapy and disease progression in hepatitis C virus (HCV) infected patients differs among individuals, suggesting a possibility of a contribution of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS1), an important component of the innate immune system with a proven antiviral function, may therefore have a relationship with the response to interferon therapy and clinical course of HCV disease. Our aim was to determine the frequency of single nucleotide polymorphism (SNP) at exon 7 splice acceptor site (SAS) of the OAS1 gene in relation to the interferon response and status of HCV infection.</p><p><hi rend="bold">Methods: </hi> A 203 bp fragment containing exon 7 SAS was amplified in 70 HCV chronic patients and 50 healthy controls. SNP was examined using restriction fragment length polymorphism (RFLP) genotyping method. Correlations of SNP genotypes with response to interferon and clinical status of patients were statistically analyzed.</p><p><hi rend="bold">Results: </hi> There was an increasing trend of response from AA to AG to GG genotypes (<hi rend="italic">P</hi> = 0.007). Genotype AA was associated with non‐response to interferon and higher degree of liver fibrosis (<hi rend="italic">P</hi> = 0.05). Multivariate analysis showed this SNP as independent and a significant determinant of the outcome of interferon therapy (odds ratio 4.913 [95% confidence interval 1.365–8.2], <hi rend="italic">P</hi> = 0.006).</p><p><hi rend="bold">Conclusions: </hi> This is the first study to show a significant association between the functional SNP at exon 7 SAS of OAS1 gene and the viral response to interferon in chronic HCV patients. Patients with AA genotype were associated with progressive HCV disease and viral resistance to interferon therapy. This OAS SNP is a potential bio‐marker to predict IFN response in chronic hepatitis C patients.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">Hepatitis C virus</term><term xml:id="k2">liver fibrosis</term><term xml:id="k3">OAS1</term><term xml:id="k4">response to interferon therapy</term><term xml:id="k5">single nucleotide polymorphism</term></keywords><keywords rend="tocHeading1"><term>Clinical Hepatology</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-NQ0KCM1W-6/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 Asia</publisherName><publisherLoc>Melbourne, Australia</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1440-1746</doi><issn type="print">0815-9319</issn><issn type="electronic">1440-1746</issn><idGroup><id type="product" value="JGH"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="JOURNAL OF GASTROENTEROLOGY HEPATOLOGY">Journal of Gastroenterology and Hepatology</title></titleGroup></publicationMeta><publicationMeta level="part" position="05105"><doi origin="wiley">10.1111/jgh.2011.26.issue-5</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue" number="5">5</numbering></numberingGroup><coverDate startDate="2011-05">May 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="13" status="forIssue"><doi origin="wiley">10.1111/j.1440-1746.2010.06605.x</doi><idGroup><id type="unit" value="JGH6605"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="tocHeading1">Clinical Hepatology</title></titleGroup><copyright>© 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.4.8 mode:FullText" date="2011-04-13"></event><event type="publishedOnlineAccepted" date="2010-12-23"></event><event type="publishedOnlineFinalForm" date="2011-04-13"></event><event type="firstOnline" date="2011-04-13"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-30"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-30"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="843">843</numbering><numbering type="pageLast" number="850">850</numbering></numberingGroup><correspondenceTo>Dr Noha Bader El Din, Department of Microbial Biotechnology, National Research Center, El‐Behooth Street 12622, Dokki, Giza 12622, Egypt. Email: <email>nbadereldin@yahoo.com</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JGH.JGH6605.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication 9 December 2010.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="4"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="47"></count><count type="wordTotal" number="6305"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Single nucleotide polymorphism at exon 7 splice acceptor site of OAS1 gene determines response of hepatitis C virus patients to interferon therapy</title><title type="shortAuthors">MK El Awady <i>et al</i>.</title><title type="short">OAS1 as marker for HCV response to interferon</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Mostafa K</givenNames><familyName>El Awady</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Mohamed A</givenNames><familyName>Anany</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>Gamal</givenNames><familyName>Esmat</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a2"><personName><givenNames>Naglaa</givenNames><familyName>Zayed</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Ashraf A</givenNames><familyName>Tabll</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a5"><personName><givenNames>Amr</givenNames><familyName>Helmy</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a3"><personName><givenNames>Abdel Rahman</givenNames><familyName>El Zayady</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a6"><personName><givenNames>Mohga S</givenNames><familyName>Abdalla</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a6"><personName><givenNames>Hayat M</givenNames><familyName>Sharada</familyName></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a2"><personName><givenNames>Maissa</givenNames><familyName>El Raziky</familyName></personName></creator><creator creatorRole="author" xml:id="cr11" affiliationRef="#a2"><personName><givenNames>Wafaa</givenNames><familyName>El Akel</familyName></personName></creator><creator creatorRole="author" xml:id="cr12" affiliationRef="#a4"><personName><givenNames>Shadia</givenNames><familyName>Abdalla</familyName></personName></creator><creator creatorRole="author" xml:id="cr13" affiliationRef="#a1" corresponding="yes"><personName><givenNames>Noha G</givenNames><familyName>Bader El Din</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="EG"><unparsedAffiliation>Department of Microbial Biotechnology, National Research Center, Egypt</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="EG"><unparsedAffiliation>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="EG"><unparsedAffiliation>Cairo Liver Center, Egypt</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="EG"><unparsedAffiliation>Department of Clinical Pathology, El Sahel Teaching Hospital, Cairo, Egypt</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="EG"><unparsedAffiliation>National Liver Institute, Shebeen El Kom, EL Monufea, Egypt</unparsedAffiliation></affiliation><affiliation xml:id="a6" countryCode="EG"><unparsedAffiliation>Faculty of Sciences Helwan University, Helwan, Egypt</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Hepatitis C virus</keyword><keyword xml:id="k2">liver fibrosis</keyword><keyword xml:id="k3">OAS1</keyword><keyword xml:id="k4">response to interferon therapy</keyword><keyword xml:id="k5">single nucleotide polymorphism</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p><b>Background and Aim: </b> Response to interferon therapy and disease progression in hepatitis C virus (HCV) infected patients differs among individuals, suggesting a possibility of a contribution of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS1), an important component of the innate immune system with a proven antiviral function, may therefore have a relationship with the response to interferon therapy and clinical course of HCV disease. Our aim was to determine the frequency of single nucleotide polymorphism (SNP) at exon 7 splice acceptor site (SAS) of the OAS1 gene in relation to the interferon response and status of HCV infection.</p><p><b>Methods: </b> A 203 bp fragment containing exon 7 SAS was amplified in 70 HCV chronic patients and 50 healthy controls. SNP was examined using restriction fragment length polymorphism (RFLP) genotyping method. Correlations of SNP genotypes with response to interferon and clinical status of patients were statistically analyzed.</p><p><b>Results: </b> There was an increasing trend of response from AA to AG to GG genotypes (<i>P</i> = 0.007). Genotype AA was associated with non‐response to interferon and higher degree of liver fibrosis (<i>P</i> = 0.05). Multivariate analysis showed this SNP as independent and a significant determinant of the outcome of interferon therapy (odds ratio 4.913 [95% confidence interval 1.365–8.2], <i>P</i> = 0.006).</p><p><b>Conclusions: </b> This is the first study to show a significant association between the functional SNP at exon 7 SAS of OAS1 gene and the viral response to interferon in chronic HCV patients. Patients with AA genotype were associated with progressive HCV disease and viral resistance to interferon therapy. This OAS SNP is a potential bio‐marker to predict IFN response in chronic hepatitis C patients.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Single nucleotide polymorphism at exon 7 splice acceptor site of OAS1 gene determines response of hepatitis C virus patients to interferon therapy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>OAS1 as marker for HCV response to interferon</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Single nucleotide polymorphism at exon 7 splice acceptor site of OAS1 gene determines response of hepatitis C virus patients to interferon therapy</title></titleInfo><name type="personal"><namePart type="given">Mostafa K</namePart><namePart type="family">El Awady</namePart><affiliation>Department of Microbial Biotechnology, National Research Center, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mohamed A</namePart><namePart type="family">Anany</namePart><affiliation>Department of Microbial Biotechnology, National Research Center, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gamal</namePart><namePart type="family">Esmat</namePart><affiliation>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Naglaa</namePart><namePart type="family">Zayed</namePart><affiliation>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ashraf A</namePart><namePart type="family">Tabll</namePart><affiliation>Department of Microbial Biotechnology, National Research Center, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Amr</namePart><namePart type="family">Helmy</namePart><affiliation>National Liver Institute, Shebeen El Kom, EL Monufea, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Abdel Rahman</namePart><namePart type="family">El Zayady</namePart><affiliation>Cairo Liver Center, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mohga S</namePart><namePart type="family">Abdalla</namePart><affiliation>Faculty of Sciences Helwan University, Helwan, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hayat M</namePart><namePart type="family">Sharada</namePart><affiliation>Faculty of Sciences Helwan University, Helwan, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maissa</namePart><namePart type="family">El Raziky</namePart><affiliation>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wafaa</namePart><namePart type="family">El Akel</namePart><affiliation>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shadia</namePart><namePart type="family">Abdalla</namePart><affiliation>Department of Clinical Pathology, El Sahel Teaching Hospital, Cairo, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Noha G</namePart><namePart type="family">Bader El Din</namePart><affiliation>Department of Microbial Biotechnology, National Research Center, Egypt</affiliation><affiliation>E-mail: nbadereldin@yahoo.com</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 Asia</publisher><place><placeTerm type="text">Melbourne, Australia</placeTerm></place><dateIssued encoding="w3cdtf">2011-05</dateIssued><edition>Accepted for publication 9 December 2010.</edition><copyrightDate encoding="w3cdtf">2011</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">4</extent><extent unit="formulas">0</extent><extent unit="references">47</extent><extent unit="linksCrossRef">0</extent><extent unit="words">6305</extent></physicalDescription><abstract lang="en">Background and Aim: Response to interferon therapy and disease progression in hepatitis C virus (HCV) infected patients differs among individuals, suggesting a possibility of a contribution of host genetic factors. 2′‐5′‐oligoadenylate synthetase 1 (OAS1), an important component of the innate immune system with a proven antiviral function, may therefore have a relationship with the response to interferon therapy and clinical course of HCV disease. Our aim was to determine the frequency of single nucleotide polymorphism (SNP) at exon 7 splice acceptor site (SAS) of the OAS1 gene in relation to the interferon response and status of HCV infection. Methods: A 203 bp fragment containing exon 7 SAS was amplified in 70 HCV chronic patients and 50 healthy controls. SNP was examined using restriction fragment length polymorphism (RFLP) genotyping method. Correlations of SNP genotypes with response to interferon and clinical status of patients were statistically analyzed. Results: There was an increasing trend of response from AA to AG to GG genotypes (P = 0.007). Genotype AA was associated with non‐response to interferon and higher degree of liver fibrosis (P = 0.05). Multivariate analysis showed this SNP as independent and a significant determinant of the outcome of interferon therapy (odds ratio 4.913 [95% confidence interval 1.365–8.2], P = 0.006). Conclusions: This is the first study to show a significant association between the functional SNP at exon 7 SAS of OAS1 gene and the viral response to interferon in chronic HCV patients. Patients with AA genotype were associated with progressive HCV disease and viral resistance to interferon therapy. This OAS SNP is a potential bio‐marker to predict IFN response in chronic hepatitis C patients.</abstract><subject lang="en"><genre>keywords</genre><topic>Hepatitis C virus</topic><topic>liver fibrosis</topic><topic>OAS1</topic><topic>response to interferon therapy</topic><topic>single nucleotide polymorphism</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Gastroenterology and Hepatology</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">0815-9319</identifier><identifier type="eISSN">1440-1746</identifier><identifier type="DOI">10.1111/(ISSN)1440-1746</identifier><identifier type="PublisherID">JGH</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>843</start><end>850</end><total>8</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>Peginterferon alfa‐2b plus ribavirin compared with interferon alfa‐2b plus ribavirin for initial treatment of chronic hepatitis C: a randomised trial</title></titleInfo><name type="personal"><namePart type="given">MP</namePart><namePart type="family">Manns</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JG</namePart><namePart type="family">McHutchison</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SC</namePart><namePart type="family">Gordon</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Manns MP, McHutchison JG, Gordon SC et al. 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