Single nucleotide polymorphism at exon 7 splice acceptor site of OAS1 gene determines response of hepatitis C virus patients to interferon therapy
Identifieur interne : 002216 ( Main/Exploration ); précédent : 002215; suivant : 002217Single 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 [Égypte] ; Mohamed A. Anany [Égypte] ; Gamal Esmat [Égypte] ; Naglaa Zayed [Égypte] ; Ashraf A. Tabll [Égypte] ; Amr Helmy [Égypte] ; Abdel Rahman El Zayady [Égypte] ; Mohga S. Abdalla [Égypte] ; Hayat M. Sharada [Égypte] ; Maissa El Raziky [Égypte] ; Wafaa El Akel [Égypte] ; Shadia Abdalla [Égypte] ; Noha G. Bader El Din [Égypte]Source :
- 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.
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DOI: 10.1111/j.1440-1746.2010.06605.x
Affiliations:
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El Awady</name><affiliation wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Department of Microbial Biotechnology, National Research Center</wicri:regionArea><wicri:noRegion>National Research Center</wicri:noRegion></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 wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Department of Microbial Biotechnology, National Research Center</wicri:regionArea><wicri:noRegion>National Research Center</wicri:noRegion></affiliation></author><author><name sortKey="Esmat, Gamal" sort="Esmat, Gamal" uniqKey="Esmat G" first="Gamal" last="Esmat">Gamal Esmat</name><affiliation wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini</wicri:regionArea><wicri:noRegion>Kasr El Aini</wicri:noRegion></affiliation></author><author><name sortKey="Zayed, Naglaa" sort="Zayed, Naglaa" uniqKey="Zayed N" first="Naglaa" last="Zayed">Naglaa Zayed</name><affiliation wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini</wicri:regionArea><wicri:noRegion>Kasr El Aini</wicri:noRegion></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 wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Department of Microbial Biotechnology, National Research Center</wicri:regionArea><wicri:noRegion>National Research Center</wicri:noRegion></affiliation></author><author><name sortKey="Helmy, Amr" sort="Helmy, Amr" uniqKey="Helmy A" first="Amr" last="Helmy">Amr Helmy</name><affiliation wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>National Liver Institute, Shebeen El Kom, EL Monufea</wicri:regionArea><wicri:noRegion>EL Monufea</wicri:noRegion></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 wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Cairo Liver Center</wicri:regionArea></affiliation></author><author><name sortKey="Abdalla, Mohga S" sort="Abdalla, Mohga S" uniqKey="Abdalla M" first="Mohga S" last="Abdalla">Mohga S. 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Sharada</name><affiliation wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Faculty of Sciences Helwan University, Helwan</wicri:regionArea><wicri:noRegion>Helwan</wicri:noRegion></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 wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini</wicri:regionArea><wicri:noRegion>Kasr El Aini</wicri:noRegion></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 wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Department of Tropical Medicine Gastroenterology and Liver Diseases, Kasr El Aini</wicri:regionArea><wicri:noRegion>Kasr El Aini</wicri:noRegion></affiliation></author><author><name sortKey="Abdalla, Shadia" sort="Abdalla, Shadia" uniqKey="Abdalla S" first="Shadia" last="Abdalla">Shadia Abdalla</name><affiliation wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Department of Clinical Pathology, El Sahel Teaching Hospital, Cairo</wicri:regionArea><wicri:noRegion>Cairo</wicri:noRegion></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 wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Department of Microbial Biotechnology, National Research Center</wicri:regionArea><wicri:noRegion>National Research Center</wicri:noRegion></affiliation><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><affiliations><list><country><li>Égypte</li></country></list><tree><country name="Égypte"><noRegion><name sortKey="El Awady, Mostafa K" sort="El Awady, Mostafa K" uniqKey="El Awady M" first="Mostafa K" last="El Awady">Mostafa K. El Awady</name></noRegion><name sortKey="Abdalla, Mohga S" sort="Abdalla, Mohga S" uniqKey="Abdalla M" first="Mohga S" last="Abdalla">Mohga S. Abdalla</name><name sortKey="Abdalla, Shadia" sort="Abdalla, Shadia" uniqKey="Abdalla S" first="Shadia" last="Abdalla">Shadia Abdalla</name><name sortKey="Anany, Mohamed A" sort="Anany, Mohamed A" uniqKey="Anany M" first="Mohamed A" last="Anany">Mohamed A. Anany</name><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><name sortKey="El Akel, Wafaa" sort="El Akel, Wafaa" uniqKey="El Akel W" first="Wafaa" last="El Akel">Wafaa El Akel</name><name sortKey="El Raziky, Maissa" sort="El Raziky, Maissa" uniqKey="El Raziky M" first="Maissa" last="El Raziky">Maissa El Raziky</name><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><name sortKey="Esmat, Gamal" sort="Esmat, Gamal" uniqKey="Esmat G" first="Gamal" last="Esmat">Gamal Esmat</name><name sortKey="Helmy, Amr" sort="Helmy, Amr" uniqKey="Helmy A" first="Amr" last="Helmy">Amr Helmy</name><name sortKey="Sharada, Hayat M" sort="Sharada, Hayat M" uniqKey="Sharada H" first="Hayat M" last="Sharada">Hayat M. Sharada</name><name sortKey="Tabll, Ashraf A" sort="Tabll, Ashraf A" uniqKey="Tabll A" first="Ashraf A" last="Tabll">Ashraf A. Tabll</name><name sortKey="Zayed, Naglaa" sort="Zayed, Naglaa" uniqKey="Zayed N" first="Naglaa" last="Zayed">Naglaa Zayed</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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