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  • Title: [Genotype distribution of chronic hepatitis B and hepatitis C patients and investigation of the resistance patterns in hepatitis B cases].
    Author: Kalayci R, Altindiş M, Gülamber G, Demirtürk N, Akcan Y, Demirdal T.
    Journal: Mikrobiyol Bul; 2010 Apr; 44(2):237-43. PubMed ID: 20549958.
    Abstract:
    The high genetic diversity in hepatitis B and C viruses (HBV and HCV, respectively), and the presence of differences in pathogenicity and response to therapy, necessitates continous monitorization of the genotypes and antiviral resistance patterns. The aims of this study were to investigate the genotype distribution of HBV and HCV in chronically infected patients and to detect the resistance patterns of HBV strains in treatment-naive patients and those under lamivudine (LAM) treatment. A total of 44 chronic hepatitis B (CHB) patients (mean age: 42 +/- 13.6 years; 31 were male) and 30 chronic hepatitis C (CHC) patients (mean age: 47 +/- 12.4 years; 8 were male) were included to this study which was carried on between September 2007-March 2008. Mutational analysis and antiviral drug resistance studies were performed by sequence analysis (ABI PRISM 310 Genetic Analyzer; Applied Biosystems, USA), with the use of the region between 80-260 codons in HBV DNA polymerase gene, and the genotype determining sequences in 5' non-coding region in HCV genome. As a result, all of the 44 CHB patients (100%) were found to be infected with HBV genotype D, while genotype 1 (26/30; 86.6%) was found to be the predominant HCV genotype in CHC patients. The frequency of HCV genotypes were as follows; 63.3% (n = 19) genotype 1b, 20% (n = 6) 1a, 13.3% (n = 4) 4a and 3.3% (n = 1) 1c. Various mutations were detected in 34.1% (15/44) of CHB patients and these were identified as M2041 (n = 6), Q215S (n = 2), L801 + M2041 (n = 1), L80V + M2041 (n = 1), Q215S + M2041 (n = 1) and M2041 + L180M (n = 1) mutations responsible for LAM resistance; V214A (n = 1) and A181T + N236T (n = 1) mutations responsible for adefovir (ADV) resistance, and V84M + V173L (n = 1) mutation responsible for ADV + LAM resistance. In 12% (3/25) of the treatment-naive CHB patients LAM resistance was detected. However, total antiviral resistance rate was found 63.2% (12/19) for CHB patients (LAM resistance in 9, ADV resistance in 2, and LAM + ADV resistance in 1 patient) who were currently under LAM treatment. Accordingly, total LAM resistance in our CHB cases was 27.3% (6.8% primary and 20.5% secondary resistance), ADV resistance was 4.5% and multidrug (LAM + ADV) resistance was 2.3%. It was concluded that, our data would be helpful in the diagnosis and management of patients with chronic liver diseases due to viral hepatitis in our region.
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