literature

HBV mutation literature information.

Detection of circulating hepatitis B virus immune escape and polymerase mutants among HBV-positive patients attending Institut Pasteur de Bangui, Central African Republic.

PMID: 31682960 2020 International journal of infectious diseases

Discussion: In addition to the three IEMs identified, several surface protein mutations were identified (sP56Q, sT57I, sN59S, sP62L, sI110L, sS140T, sE164G, sS207N, and sL216*), which have also been reported in previous studies (Mello et al.,; Lin et al.,; Munshi et al.,; Qin and Liao,).

A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1.

PMID: 30870427 2019 PloS one

Figure: A nonsense mutation at the codons for L95, W182 and L216 resulted in sL95*, sW182* and sL216*, respectively.

Discussion: The three nonsense mutants, designated sL95*, sW182* and sL216*, have been shown to have oncogenic property and sW182* was the most potent.

Clinical and Virological Aspects of HBV Reactivation: A Focus on Acute Liver Failure.

PMID: 31527514 2019 Viruses

Discussion: HBsAg stop codon mutations leading to a truncated HBsAg such as W172* have been described in patients with chronic hepatitis B patients in the past and have been associated with lamivudine/entecavir resistance, cirrhosis, and hepatocellular carcinoma, as well as defective HBsAg secretion like L216*.

Discussion: Furthermore, the sequencing of the whole HBV genome per NGS and the functional analysis of the Discussion: One of them, the SHB L216* mutation, was associated with reduced HBsAg production and secretion.

High rates of chronic HBV genotype E infection in a group of migrants in Italy from West Africa: Virological characteristics associated with poor immune clearance.

PMID: 29596494 2018 PloS one

Result: A similar situation was observed also for patients 2 and 3, and it was characterized by specific mutational profiles (L49R+S193L and G102A/G+S193S/L+S210S/R+L216 stop) observed only in plasma and not in liver tissue (Fig 3).

Identification of transforming hepatitis B virus S gene nonsense mutations derived from freely replicative viruses in hepatocellular carcinoma.

PMID: 24587012 2014 PloS one

Abstract: Three nonsense mutations of S gene (sL95*, sW182*, and sL216*) were identified in the HBcAg(+) HCC tumor tissues.

Discussion: On the other hand, three nonsense mutations of S gene were found in the cancerous part (

Discussion: The other two S truncation mutants, sL95* and sL216*, also found to had transformation activities, though weaker than sW182*.

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