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Mutations within enhancer II and BCP regions of hepatitis B virus in relation to advanced liver diseases in patients infected with subgenotype B3 in Indonesia

✍ Scribed by Didik Setyo Heriyanto; Yoshihiko Yano; Takako Utsumi; Nungki Anggorowati; Hanggoro Tri Rinonce; Maria Inge Lusida; Soetjipto; Catharina Triwikatmani; Neneng Ratnasari; Sutanto Maduseno; Putut Bayu Purnama; Siti Nurdjanah; Yoshitake Hayashi


Publisher
John Wiley and Sons
Year
2011
Tongue
English
Weight
111 KB
Volume
84
Category
Article
ISSN
0146-6615

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✦ Synopsis


Abstract

Studies on the characteristics of mutations within the hepatitis B virus (HBV) genome, their roles in the pathogenesis of advanced liver diseases, and the involvement of host properties of HBV‐infected individuals have not been conducted in subgenotype B3‐infected populations. For addressing this issue, 40 cases with HBV surface antigen (HBsAg)—positive advanced liver diseases, including advanced liver cancer and cirrhosis (male 31, female 9, age 54.4 ± 11.6‐year‐old), were collected and compared with 109 cases with chronic hepatitis B (male 71, female 38, age 38.0 ± 13.4‐year‐old). Mutations in enhancer II (Enh II) and basal core promoter (BCP)/precore regions were analyzed by PCR‐direct sequencing method. HBV viral load was examined by real‐time PCR. For all examined regions, the prevalence of mutation was significantly higher in cases with advanced liver diseases. Multivariate analysis showed that, in patients older than 45 years, C1638T and T1753V mutations constituted independent risk factors for the advancement of liver diseases. The presence of C1638T and T1753V mutations may serve as predictive markers for the progression of liver diseases in Indonesia and other countries, where subgenotype B3 infection is prevalent. J. Med. Virol. 84:44–51, 2011. © 2011 Wiley Periodicals, Inc.


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