Complete nucleotide sequences of hepatitis B virus genomes associated with epidemic fulminant hepatitis

✍ Scribed by Asahina, Yasuhiro; Enomoto, Nobuyuki; Ogura, Yuki; Sakuma, Ikuo; Kurosaki, Masayuki; Izumi, Namiki; Marumo, Fumiaki; Sato, Chifumi

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 719 KB
• Volume: 48
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/(sici)1096-9071(199602)48:2<171::aid-jmv9>3.0.co;2-6

✦ Synopsis

Pre-corekore mutants are frequently observed in patients with fulminant hepatitis. To investigate the extent of molecular characteristics of hepatitis B virus (HBV) genomes implicated in the development of fulminant hepatitis, fulllength HBV genomes were sequenced directly from sera of two patients with epidemic fatal fulminant hepatitis, after amplification by the polymerase chain reaction. These two genomes, of 321 5 nucleotides, were 99.6% identical, indicating that a common source of HBV potentially caused fulminant hepatitis. Thirty unique nucleotide mutations were commonly found in the two entire HBV genomes. Three were located in the stem-loop structure, changing this element to a more stable structure. Twenty-five unique amino acid substitutions were found in each open reading frame, except for the X and presurface 2 genes. One was located in the pre-surface 1 gene; two were in the surface gene; three were in the pre-core gene, including codons 28 (tryptophan to stop codon) and 29 (glycine to aspartic acid); eight were in the core gene; and 11 were in the polymerase gene. The pre-core mutations at codons 28 and 29 were common to the two HEW strains reported previously in patients with epidemic fulminant hepatitis. Thus, HBV genornes associated with epidemic fatal fulminant hepatitis have numerous unique mutations, located mainly in the polymerase gene, as well as the pre-corekore gene, including mutations in the stem-loop structure of the pregenome encapsidation signal sequence. These mutations may be associated with the development of fulminant hepatitis. o 1996 Wiley-Liss, Inc.