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New HBV subgenotype D 9, a novel D / C recombinant, identified in patients with chronic HB e A g‐negative infection in E astern I ndia
Author(s) -
Ghosh S.,
Banerjee P.,
Deny P.,
Mondal R. K.,
Nandi M.,
RoyChoudhury A.,
Das K.,
Banerjee S.,
Santra A.,
Zoulim F.,
Chowdhury A.,
Datta S.
Publication year - 2013
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/j.1365-2893.2012.01655.x
Subject(s) - phylogenetic tree , genotype , virology , biology , hepatitis b virus , genome , genetics , hbeag , phylogenetics , virus , hbsag , gene
Summary Genome diversity is a hallmark of hepatitis B virus ( HBV ), which allowed its classification into 10 genotypes ( A – J ) and numerous subgenotypes. Among them, Genotype D is currently segregated into eight subgenotypes ( D 1– D 8). Here, we report the identification and characterization of a novel subgenotype within genotype D of HBV from chronic hepatitis B e antigen ( HB e A g)‐negative patients of E astern I ndia. Phylogenetic tree analysis based on complete genome sequences revealed that six of 39 HBV / D isolates formed a distinct cluster supported by high bootstrap value and had nucleotide divergence >4% relative to the known D subgenotypes ( D 1– D 8), justifying their assignment into a new subgenotype ( D 9). By comparing the amino acid sequences of the four ORF s of HBV / D 9 with D 1– D 8, 36 specific residues, including a unique one ( E 112 in the core region), were identified that could be considered as a signature of D 9. Further analysis by S implot, B oot S can and jp HMM demonstrated that D 9 resulted from a discrete recombination with genotype C over the precore–core region. This type of recombination has not been described previously as all C / D recombinants reported so far possessed genotype C backbones with mosaic fragments derived from HBV / D . Interestingly, compared to other subgenotypes of HBV / D , D 9 isolates had a higher frequency of mutations ( A 1762 T and G 1764 A ) in the basal core promoter region that had been implicated in the development of hepatocellular carcinoma. Further investigations are needed to determine the overall prevalence and clinical significance of these newly characterized D 9 strains and to assess the impact of inter‐genotypic recombination on viral properties.

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