BACKGROUND/AIMS: There is a paucity of information regarding hepatitis B virus (HBV) from patients with fulminant hepatitis (FH) without precore (pre-C, nt 1896) and core promoter (CP, nt 1762, 1764) mutations. METHODS: Pre-C and CP mutations were studied in eight patients with FH and 26 patients with acute hepatitis (AH) due to HBV. One patient with FH (FH1) was infected with HBV without these mutations. Interestingly, the sera of the infectious source (IS1) and of a patient with AH (AH1) infected from IS1 were available. Complete HBV genomes from these three patients were analyzed. RESULTS: These mutations were found in seven of eight FH and five of 26 AH (P<0.01). HBV from FH1, IS1 and AH1 belonged to genotype D. Nucleotide difference between FH1 and AH1 was six of 3182 bases (nt 493, 998, 1173, 2928, 3067, and 3078). Two and five substitutions of deduced amino acid sequences were found in the pre-S1 and polymerase regions, respectively. The same nucleotide substitutions at nt 493, 1173, 2928 and 3067 were found in several patients with FH in our laboratory or GenBank. CONCLUSIONS: These six nucleotide substitutions of HBV DNA could be candidates of mutations relating to FH.
BACKGROUND/AIMS: There is a paucity of information regarding hepatitis B virus (HBV) from patients with fulminant hepatitis (FH) without precore (pre-C, nt 1896) and core promoter (CP, nt 1762, 1764) mutations. METHODS: Pre-C and CP mutations were studied in eight patients with FH and 26 patients with acute hepatitis (AH) due to HBV. One patient with FH (FH1) was infected with HBV without these mutations. Interestingly, the sera of the infectious source (IS1) and of a patient with AH (AH1) infected from IS1 were available. Complete HBV genomes from these three patients were analyzed. RESULTS: These mutations were found in seven of eight FH and five of 26 AH (P<0.01). HBV from FH1, IS1 and AH1 belonged to genotype D. Nucleotide difference between FH1 and AH1 was six of 3182 bases (nt 493, 998, 1173, 2928, 3067, and 3078). Two and five substitutions of deduced amino acid sequences were found in the pre-S1 and polymerase regions, respectively. The same nucleotide substitutions at nt 493, 1173, 2928 and 3067 were found in several patients with FH in our laboratory or GenBank. CONCLUSIONS: These six nucleotide substitutions of HBV DNA could be candidates of mutations relating to FH.
Authors: Wing-Kin Sung; Hancheng Zheng; Shuyu Li; Ronghua Chen; Xiao Liu; Yingrui Li; Nikki P Lee; Wah H Lee; Pramila N Ariyaratne; Chandana Tennakoon; Fabianus H Mulawadi; Kwong F Wong; Angela M Liu; Ronnie T Poon; Sheung Tat Fan; Kwong L Chan; Zhuolin Gong; Yujie Hu; Zhao Lin; Guan Wang; Qinghui Zhang; Thomas D Barber; Wen-Chi Chou; Amit Aggarwal; Ke Hao; Wei Zhou; Chunsheng Zhang; James Hardwick; Carolyn Buser; Jiangchun Xu; Zhengyan Kan; Hongyue Dai; Mao Mao; Christoph Reinhard; Jun Wang; John M Luk Journal: Nat Genet Date: 2012-05-27 Impact factor: 38.330
Authors: Maria Alma Bracho; María José Gosalbes; Francisco González; Andrés Moya; Fernando González-Candelas Journal: J Clin Microbiol Date: 2006-04 Impact factor: 5.948