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      Evolution of HBV S‐gene in the backdrop of HDV co‐infection

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      https://www.riss.kr/link?id=O119686569

      • 저자
      • 발행기관
      • 학술지명
      • 권호사항
      • 발행연도

        2018년

      • 작성언어

        -

      • Print ISSN

        0146-6615

      • Online ISSN

        1096-9071

      • 등재정보

        SCI;SCIE;SCOPUS

      • 자료형태

        학술저널

      • 수록면

        1328-1336   [※수록면이 p5 이하이면, Review, Columns, Editor's Note, Abstract 등일 경우가 있습니다.]

      • 소장기관
      • 구독기관
        • 전북대학교 중앙도서관  
        • 성균관대학교 중앙학술정보관  
        • 부산대학교 중앙도서관  
        • 전남대학교 중앙도서관  
        • 제주대학교 중앙도서관  
        • 중앙대학교 서울캠퍼스 중앙도서관  
        • 인천대학교 학산도서관  
        • 숙명여자대학교 중앙도서관  
        • 서강대학교 로욜라중앙도서관  
        • 계명대학교 동산도서관  
        • 충남대학교 중앙도서관  
        • 한양대학교 백남학술정보관  
        • 이화여자대학교 중앙도서관  
        • 고려대학교 도서관  
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      부가정보

      다국어 초록 (Multilingual Abstract)

      HBV‐HDV co‐infected people have a higher chance of developing cirrhosis, fulminant hepatitis, and hepatocellular carcinoma (HCC) compared to those infected only with HBV. The present study was conducted to investigate HBV genotypes and phylogeny a...

      HBV‐HDV co‐infected people have a higher chance of developing cirrhosis, fulminant hepatitis, and hepatocellular carcinoma (HCC) compared to those infected only with HBV. The present study was conducted to investigate HBV genotypes and phylogeny among HBV mono‐infected and HBV‐HDV co‐infected patients, as well as analyze mutations in the surface gene of HBV in mono‐infected and co‐infected patients. A total of 100 blood samples (50 co‐infected with HBV and HDV, and 50 mono‐infected with HBV only) were collected for this study. HBV DNA was extracted from patient sera and partial surface antigen gene was amplified from HBV genome using polymerase chain reaction. HBV S gene was sequenced from 49 mono‐infected and 36 co‐infected patients and analyzed to identify HBV genotypes and phylogenetic patterns. Subsequently, HBV S amino acid sequences were analyzed for mutational differences between sequences from mono‐ and co‐infected patients. HBV genotype D was predominantly found in both mono‐infected as well as co‐infected patients. Phylogenetic analysis showed the divergence of HBV sequences, between mono‐ and co‐infected patients, into two distinct clusters. HBV S gene mutation analysis revealed certain mutations in HBV‐HDV co‐infected subjects to be distinct from those found in mono‐infected patients. This might indicate the evolution of HBV S gene under selection pressures generated from HDV coinfection.

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