Precore/core mutations of hepatitis B virus genotype D arising in different states of infection.
PMID: 35415256
2022
Clinical and experimental hepatology
Abstract: Results: The stop codon of W28*(G1896A) was determined as the most prevalent mutation (55%) of the precore region.
Discussion: The result of our study showed that a precore point mutation, G1896A, that converts the tryptophan to a stop codon (W28*), was the most common variation in the patients, as detected in chronic HBV in Asia and the Mediterranean region.
Discussion: reported that 31.8% (14/44) of patients had mutations in the precore region (G1896A).
Regulatory function of interferon-inducible 44-like for hepatitis B virus covalently closed circular DNA in primary human hepatocytes.
Abstract: METHODS: Primary human hepatocytes were infected with HBV using genomic plasmids carrying the basic core promoter mutation A1762T/G1764A and/or the precore mutation G1896A and treated with IFN-gamma and IFN-alpha.
Combining the HBcrAg decline and HBV mutations predicts spontaneous HBeAg seroconversion in chronic hepatitis B patients during the immune clearance phase.
Abstract: Baseline A1574T, G1862A, G1896A, and C1913G mutations and HBcrAg levels with a sharp decrease at Week 28 were associated with spontaneous HBeAg seroconversion.
Abstract: The mutation frequencies of A1574T (51.11% vs. 18.18%, p = 0.001), G1862A (30.00% vs. 13.03%, p = 0.001), G1896A (27.22% vs. 5.45%, p = 0.001), and C1913G (32.78% vs. 12.73%, p = 0.001) in Group A were significantly higher than Group B.
Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran.
Result: Moreover, a G to A substitution at nucleotide position 1896 (G1896A) was detected in the pre-C region of one sample (HB55) (S2 Fig), this sample was negative for HBeAg.
Discussion: Notably, the sample with G1896A mutation was HBeAg negative.
Discussion: Of these, the pre-C mutation (G1896A) eliminates HBeAg expression at the translational level, whereas BCP mutations (G1764A) decrease HBeAg expression at the transcriptional level.
Discussion: The G1896A mutation causes the conversion of TGG TAG (Tr
Reactivation of Occult Hepatitis B Virus Infection During Long-Term Entecavir Antiviral Therapy.
Abstract: Genetic sequencing of HBV showed the mutants of S143T, D144G, and G145R in the S gene region, and the mutant of site 1896 in the pre-Core region coexisted with the w
Result: Mutation analysis of this patient's HBV showed there were three mutants (S143T, D144G, and G145R) in the S gene region, and the mutant of site 1896 in the pre-Core region coexisted with the wild type (G1896A/G), but no mutation in the pre-S1, pre-S2, and BCP gene regions (Details shown in Table 3).
Molecular characteristics of HBV infection among blood donors tested HBsAg reactive in a single ELISA test in southern China.
Discussion: G1896A is another typical mutation in the pre-C region, which generates a stop codon at the 28th amino acid position of the HBeAg sequence, resulting in the inhibition of protein synthesis.
The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report.
Discussion: However, G1896A or A1762T/G1764A mutations were not found in this patient with genotype C HBV by DNA sequencing, while A1727T, C1730G and C1799G mutations were found in BCP region, which were reported to be associated significantly with cirrhosis.
Specific determination of hepatitis B e antigen by antibodies targeting precore unique epitope facilitates clinical diagnosis and drug evaluation against hepatitis B virus infection.
Abstract: In contrast to widely used commercial assays, the NTR-HBeAg completely eliminated the cross-reactivity with secreted HBcAg from precore mutant (G1896A) virus in either cell culture or patient sera.
Method: To produce HBeAg of various genotypes, a serial of HBV 1.3-fold or CMV-driven 1.1-fold genome plasmids with genotypes A-I (detailed information was shown in supplemental Table 1) or with precore G1896A mutation were transfected into HepG2 cells or Huh7 cells using X-tremeGENE HP DNA Transfection Reagent (Roche).
Result: As HBV genotype G permanently harbours C1817T and G1896A nonsense mutations in the precor
Amino Acid Polymorphism in Hepatitis B Virus Associated With Functional Cure.
PMID: 34352407
2021
Cellular and molecular gastroenterology and hepatology
Method: This clone has the amino acid substitution G1896A, which prevents HBeAg production.
Transcriptome analysis of hepatoma cells transfected with Basal Core Promoter (BCP) and Pre-Core (PC) mutant hepatitis B virus full genome construct.
PMID: 33595430
2021
The Journal of general virology
Abstract: Infections with Basal Core Promoter (BCP) (A1762T/G1764A) and Pre-Core (PC) (G1896A) hepatitis B virus HBeAg mutants are associated with severe liver injury.
HBV mutation literature information.
PMID: 
2022
Clinical and experimental hepatology
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