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      A new core promoter mutation and premature stop codon in the S gene in HBV strains from Iranian patients with cirrhosis.

      Journal of Viral Hepatitis
      Adult, Cluster Analysis, Codon, Nonsense, DNA, Viral, genetics, Female, Fibrosis, virology, Genotype, Hepatitis B, complications, Hepatitis B Core Antigens, Hepatitis B Surface Antigens, blood, Hepatitis B virus, isolation & purification, Humans, Iran, Male, Middle Aged, Molecular Epidemiology, Molecular Sequence Data, Mutagenesis, Insertional, Mutation, Phylogeny, Promoter Regions, Genetic, Sequence Analysis, DNA, Sequence Deletion, Sequence Homology, Viral Load

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          Abstract

          In order to define hepatitis B virus (HBV) mutational patterns in Iran, nucleotide sequences obtained from 91 patients and encompassing the precore, basal core promoter (BCP) and surface (S) regions, were compared. The patients were grouped as asymptomatic carriers, chronic active hepatitis or cirrhotic patients. Genotypes and mutations were determined by sequencing and phylogenetic analysis. All strains belonged to genotype D, and most of them to subgenotype D1. All but two strains specified ayw2, one ayw3 and one adw2 determinants. Two deletions of 8- or 20-bp were found in the X region in eight strains, six from patients with chronic active hepatitis. Eight of 21 strains from patients with cirrhosis harboured unusual mutations such as a stop codon at position 69 in the S region or a previously not described mutation in the BCP region ((1761)TC/ATTTG(1766)). All patients infected by strains with the stop codon mutation had detectable HBsAg and high viral load. The accumulation of mutations found in the BCP and S regions in HBV strains from patients with chronic active hepatitis and cirrhosis may predict disease progression in Iranian HBsAg carriers.

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