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 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
Abstract: A mutation in C-region of HBsAg (L216*), was associated with reduced HBsAg production and secretion.
Abstract: An HBsAg mutation (L216*) was found to be more frequent in ALF patients and was associated with reduced HBsAg production and secretion.
Method: A stop codon mutation was found more frequently in the ALF group (SHB L216*, see Table 3) and was selected for further analysis.


  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: sW182* and sL216* were recurrently found in the 25 HBcAg (-) HCC tumor tissue, too.
Abstract: Three nonsense mutations of S gene (sL95*, sW182*, and sL216*) were identified in the HBcAg(+) HCC tumor tissues.
Method: To construct plasmids encoding truncated preS/S proteins containing 3 nonsense mutations, s<



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