HBV whole-genome mutation profile in HIV-1/HBV coinfected patients in a long-term follow-up study.

Journal Article (Journal Article)

PURPOSE: Human immunodeficiency virus (HIV-1)-infected patients frequently harbour hepatitis B and C viruses (HBV and HCV, respectively). Possible modifications of the natural history of hepatitis B may occur. The aim of this study was to characterise HBV diversity and evolutionary and mutational viral genome profiles in HIV-1/HBV coinfections. METHODS: HIV-1 and HBV markers determinations (Roche, FRG; Abbott, USA) and HBV genome-length retrospective analysis were performed in follow-up isolates from patients who were either stably HBsAg-negative with a low level of HBV DNA (occult hepatitis B infection, OBI) or HBsAg-positive with a high level of HBV DNA. Phylogenetic analysis (maximum likelihood method, MEGA5), statistical analysis and evolutionary rates calculation (d S/d N) were applied. RESULTS: Positive selection pressures in the PreS/S region and a significantly higher number of mutations in this region including the major hydrophilic region (MHR) and the "a" determinant were shown in HBsAg-negative (possibly OBI) compared to stably HBsAg-positive HIV-1/HBV subgenotypes D3/A2 coinfected patients. Mutants previously described in HIV-1/HBV coinfected patients were found. Known mutants Y100C, P127T and P120A associated to Y134H and S143T and new S mutants, which may potentially affect HBsAg expression and secretion and anti-HBs binding, were detected in baseline sera persisting up to the end of 9 years follow-up. Known mutations of BCP, Pre-C, C and X regions were also characterised. Natural mutants strictly known as being involved in diagnostic failure were not detected; however, numerous corresponding sites showed amino acid variations. CONCLUSIONS: Evolutionary and genotypic differences observed, particularly in the PreS/S region, between HBsAg-negative (OBI) and HBsAg-positive HIV-1/HBV coinfected patients, may contribute, in association with mutations of other genomic regions, to the HBsAg-negative phenotype.

Full Text

Duke Authors

Cited Authors

  • Taffon, S; Genovese, D; Blasi, M; Pierotti, P; Degli Esposti, A; Catone, S; Chionne, P; Pulimanti, B; Candido, A; Dettori, S; Tosti, ME; Argentini, C; Mazzotta, F; Rapicetta, M

Published Date

  • August 2014

Published In

Volume / Issue

  • 42 / 4

Start / End Page

  • 675 - 687

PubMed ID

  • 24700252

Electronic International Standard Serial Number (EISSN)

  • 1439-0973

Digital Object Identifier (DOI)

  • 10.1007/s15010-014-0616-2


  • eng

Conference Location

  • Germany