literature

Precore/core mutations of hepatitis B virus genotype D arising in different states of infection.

PMID: 35415256 2022 Clinical and experimental hepatology

Introduction: In a study conducted in the Korean population, the five HBcAg mutations P5H/L/T, E83D, I97F/L, L100I, and Q182K/Stop were significantly more frequent in subjects with chronic hepatitis and cirrhosis.

Discussion: However, in spite of their prevalence, our data showed that E80Q/D, E113D/Q, S181P/R and Q182K/*Stop variations were not statistically significantly different among the groups.

Discussion: There were some variations such as E77Q,

PMID: 33803998 2021 Microorganisms

Abstract: We also found that there are a total of 19 signature single nucleotide polymorphisms (SNPs), of which 2 and 17 nonsynonymous mutation types were specific to rt269L and rt269I, respectively: Of these, most are HBeAg negative infections (preC-W28*, X-V5M and V131I), lowered HBV DNA or virion production (C-I97F/L, rtM204I/V) or preexisting nucleot(s)ide analog resistance (NAr) (rtN139K/H, rtM204I/V and

Mutations in Core Gene Region of Hepatitis B Virus in Patients with Chronic Hepatitis B.

PMID: 29739114 2018 Clinical laboratory

Abstract: Some types of mutations (V27I, R47H, Y132I, R174STOP, S181P, Q182K) were only detected in subjects with liver cirrhosis.

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

Introduction: Furthermore, five HBcAg mutations identified in a Korean population, P5H/L/T, E83D, I97F/L, L100I, and Q182K/Stop, were shown to be significantly enriched in HCC patients compared with patients at earlier disease stages, including those with cirrhosis and chronic hepatitis (Kim et al.,).

Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer.

PMID: 28373061 2017 Virus research

Result: In addition, the E180G, S181P, and Q182K missense mutations were identified in 12 clones derived from 5 HCC patients but only 3 clones from 2 non-HCC patients (Table 2).

Discussion: The C-terminal 10 residues of the core protein are dispensable for HBV replication, and the high replication capacity of clones 4.2, 4.9, 13.2, and 5.1 suggests that the E180G, S181P, and Q182K mutations present in these clones do not markedly suppress genome replication.

Discussion: These include E180G, S181P, Q182K, and

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