Precore/core mutations of hepatitis B virus genotype D arising in different states of infection.
PMID: 35415256
2022
Clinical and experimental hepatology
Table: E77Q
Discussion: The present study also demonstrated that the rates of F24Y, E64D, E77Q, L116I, and E180A mutations were higher in the C/HCC patients than the other groups; however, these differences were not st
Discussion: reported 6 core mutations (F24Y, E64D, E77Q, A80I/T/V, L116I, and E180A) related to the progression of the disease to cirrhosis and HCC.
The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease.
PMID: 30406036
2018
Frontiers in cellular and infection microbiology
Abstract: Six of the seven significant core mutations that were identified in this study were located within immuno-active epitopes; E77Q, A80I/T/V, and L116I were located within B-cell epitopes, and F24Y, E64D, and V91S/T were located within T-cell epitopes.
Abstract: Two precore mutations, W28* and G29D, and six core mutations, F24Y, E64D, E77Q, A80I/T/V, L116I, and E180A were
Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations.
Result: A polyclonal rabbit antibody (Dako) efficiently detects the wild-type core protein, but it is less reactive with the core protein of clone 4B due to an E77Q mutation (Kim K et al., unpublished).