Method: In the PC region, two nucleotide changes were analyzed: the presence of a point mutation from G to A at nucleotide 1896 (G1896A), which signals the mutant PC phenotype; and the change C to T at position 1858, which defines the C1858T mutation.
Result: The C1858T and G1757A substitutions were found in 226/228 (99.1%) and 189/228 patients (82.8%) respectively.
Discussion: In our population, the majority of PC sequences (98%) harbored the C1858T mutation.
Discussion: In our study, it was surprising to note the low preval
Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression.
5Result: All nucleotides sequences corresponding to genotypes D had a thymidine ""T"" at nt 1858, whereas all genotype A sequences had a cytosine ""C"" at nt 1858, except four cases harboring G1896A, in which concomitant C1858T mutation occurred."
Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa.
Result: The classical G1896A mutation occurred in five isolates and in four cases it occurred together with C1858T.
Discussion: The HBeAg negativity found in 44/49 Shongwe participants (89,7%) could be accounted for by the following HBV mutations: the basic core promoter mutations A1762T/G1764A, which can down-regulate transcription of precore mRNA; the Kozak sequence mutants that affect HBeAg translation; precore start codon mutations that abolish HBeAg expression, the G1862T mutation,which interferes with post-translational modification of the HBeAg-precurso
Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence.
Result: Of limited number of 1858C variant virus examined in this study, none of them was found to have 1896A mutation when mutant G1896A was associated with double mutation A1850T and C1858T.
Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis.
PMID: 19574418
2009
Journal of the National Cancer Institute
Result: Statistically si
Result: The most commonly reported HBV mutations associated with HCC risk were PreS mutations, A1762T/G1764A, G1896A, T1753V, C1653T, and C1858T.
Result: The risk estimates of HCC for PreS mutations, C1653T, T1753V, A1762T/G1764A, G1896A, and C1858T in individual case-control and cohort studies and summary estimates are shown in Figure 2.
Nucleic acid sequence analysis of basal core promoter/precore/core region of hepatitis B virus isolated from chronic carriers of the virus from Kolkata, eastern India: low frequency of mutation in the precore region.
Abstract: CONCLUSION: The pattern of core promoter and precore mutation of HBV isolates in the present study is atypical and not in accordance with reports from other parts of the world, where genotype D and genotype C with T at codon 1858 are common.
Two subtypes (subgenotypes) of hepatitis B virus genotype C: A novel subtyping assay based on restriction fragment length polymorphism.
Abstract: Some specific mutations were detected in the encapsidation signal; precore stop mutation (A1896), accompanied by a C-to-T substitution at nt 1858, was found in HBV/Ce strains, and another precore mutation (A1898), accompanied by a C-to-T mutation at nt 1856, was found in HBV/Cs.
Basal core promoter and precore mutations in the hepatitis B virus genome enhance replication efficacy of Lamivudine-resistant mutants.
Abstract: The PC mutation (G1896A+C1858T) creates a translational stop codon resulting in absent HBeAg expression, whereas BCP mutations (A1762T/G1764A) reduce HBeAg expression by transcriptional mechanisms.
Molecular analysis of hepatitis B virus genomes isolated from black African patients with fulminant hepatitis B.
Abstract: The mutation most often reported in patients with fulminant hepatitis B, the G1896A precore stop-codon substitution, was, as expected, not present in the genotype A isolates with the exception of one in which it was accompanied by a compensatory C1858T substitution.
Base-pair alterations in the epsilon-lower stem due to a novel double substitution in the precore gene of HBV-e negative variant were recovered by secondary mutations.
Abstract: The destabilized C : G base-pairing in the lower stem of epsilon-hairpin due to G1896A substitution is reportedly compensated by a second C1858T mutation and suggested to play an important role in enhanced selection of the HBe negative variant.
HBV mutation literature information.
PMID: 
2013
PloS one
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