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العنوان
an association of asingle nucleotide poly morphism within 2.5 oligoadenylate synthetase 1 gene in the human with response to interferon and ribavirin treatment in chronic hepatitis c infection /
المؤلف
mohamed, mohamed ahmed .
هيئة الاعداد
باحث / محمد احمد محمد
مشرف / مهجة شفيق عبد الله
مشرف / حياه محمد ابراهيم
مشرف / مصطفى كامل العويضي
مشرف / نهى جمال الدين سامي
تاريخ النشر
2012.
عدد الصفحات
i,vii , p79. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الكيمياء
تاريخ الإجازة
1/1/2012
مكان الإجازة
جامعة حلوان - كلية العلوم - كيمياء
الفهرس
Only 14 pages are availabe for public view

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from 94

Abstract

In conclusion human genetic differences in interferon stimulated genes (ISGs) like a SNP in OAS I at exon 7 splice-acceptor site are associated with the response to pegylated interferon- u (Peg-IFN- u) plus ribavirin therapy in HCV genotype-4 infected patients.OAS lone of the most important ISGs encoding the antiviral enzyme 2’-5’oligoadenylate synthetase (2’-5’AS) are critical components of the innate immune response to viruses. This enzyme uses adenosine triphosphate in 2’-specific nucleotidyl transfer reactions to synthesize 2’-5’-0Iigoadenylates, which activate latent ribonuclease, resulting in degradation of viral RNA and inhibition of virus replication. We studied single nucleotide polymorphism (SNP) at exon 7 splice-acceptor site iq OASI for their associations with response to pegylated interferon- u (Peg-IFN- u) plus ribavirin therapy in HCV genotype-4 infected patients. Our observations suggested that polymorphisms at exon 7 splice-acceptor site in OAS I gene may be involved in determining the outcome of HCV infection. Patients harboring GG genotype at this site tend to achieve sustained response to interferon therapy (59.4%) suggesting that the G allele conferred a better signaling towards viral clearance. On the other hand, a clear association exists between both allele A containing genotypes i.e. GA and AA and resistance to interferon therapy (62% and89% respectively). These findings confirmed earlier reports that the G allele at this acceptor site retained the splice site and was associated with a higher OAS enzyme activity (P46), whereas the A allele (AA at acceptor site) ablated the splice site and resulted in a larger molecular weight protein with a lower OAS enzyme activity (P48).
Finally, the results of the present study may have clinical and pathogenic Implications and suggest that the SNP of OAS-I at the exon 7 splice acceptor site repres
ents added value to the promising markers for prognosis of disease progression and