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ASSOCIATION OF PRE-S/S AND POLYMERASE MUTATIONS WITH ACUTE AND CHRONIC HEPATITIS B VIRUS INFECTIONS IN PATIENTS FROM RIO DE JANEIRO, BRAZIL
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Affilliation
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virologia Molecular. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Espírito Santo. Departamento de Medicina Social. Vitória, ES, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hepatites Virais. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virologia Molecular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virologia Molecular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hepatites Virais. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virologia Molecular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virologia Molecular. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Espírito Santo. Departamento de Medicina Social. Vitória, ES, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hepatites Virais. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virologia Molecular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virologia Molecular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hepatites Virais. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virologia Molecular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Virologia Molecular. Rio de Janeiro, RJ, Brasil.
Abstract
Several hepatitis B virus (HBV)-related factors, including the viral load, genotype, and
genomic mutations, have been linked to the development of liver diseases. Therefore, in this study
we aimed to investigate the influence of HBV genetic variability during acute and chronic infection
phases. A real-time nested PCR was used to detect HBV DNA in all samples (acute, n = 22; chronic,
n = 49). All samples were sequenced for phylogenetic and mutation analyses. Genotype A, subgenotype
A1, was the most common genotype in the study population. A total of 190 mutations
were found in the pre-S/S gene area and the acute profile revealed a greater number of nucleotide
mutations (p < 0.05). However, both profiles contained nucleotide mutations linked to immune escape
and an increased risk of hepatocellular carcinomas (acute, A7T; chronic, A7Q). Furthermore, 17 amino
acid substitutions were identified in the viral polymerase region, including the drug resistance
mutations lamivudine and entecavir (rtL180M), with statistically significant differences between the
mutant and wild type strains. Owing to the natural occurrence of these mutations, it is important to
screen for resistance mutations before beginning therapy.
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