Abstract: Our results show that for the subgenotype (sgt) D1, which has an 8-nucleotide deletion (sgtD1del) and exhibits lower fitness, the levels of extracellular DNA and intracellular replicative intermediates were much lower than with sgtD1wt or sgtD1mut (G1896A), which had higher fitness.
Hepatitis B virus in Mar del Plata, Argentina: Genomic characterization and evolutionary analysis of subgenotype F1b.
Abstract: A unique D3 presented the G1896A substitution at the preC (HBeAg negative phenotype).
Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients.
Method: Furthermore, mutants C18T, G82A, A115C, G120A, A138G, and C189A in SPII were cloned into a plasmid pBlueBac4.5 1.2/PC (p1.2/PC) respectively, which contained a 1.2-fold length HBV genome of genotype C2 with a G1896A mutation in the preC region.
Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors.
Discussion: Neither the precore stop codon mutation G1896A which abolishes HBeAg production or the basal core promoter mutations which cause reduced HBeAg production were found in any samples from either panel.
A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus.
Introduction: One of the most common mutations of HBV is G1896A at the precore region that converts TGG to TAG, a stop codon, which abolishes the expression of hepatitis B e antigen (HBeAg).
Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients.
Result: Although G1896A frequently disrupts the production of HBeAg via the introduction of a premature stop codon, other mutations are likely to achieve a similar clinical effect via different molecular means.
Result: Aside from C1817T and A1838G variants, it is worth mentioning that C1653T, G1896A, and G1899A displayed the next most significant association with viral load in the discovery patient cohort (LRT p = 6 x 10-8, p = 6.7 x 10-8, and p = 2.3 x 10-7, respectively).
Result: Aside from its previously mentioned role in the epsilon region of the pgRNA, G1896A introduces a stop codon in the precore region abolishing HBeAg
rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections.
Abstract: Our epidemiological study showed HBeAg negative infections of rt269I infections were attributed to a higher frequency of preC mutations at 1896 (G to A).
Result: Of the various HBV mutations, G1896A mutations on the pre-core region (preC mutation) and A1762T/G1764A double mutations on the basal core promoter (BCP) lead to HBeAg negative infection that are significantly related to liver disease progression.
Result: The Higher Frequency of preC Mutat
Next generation sequencing identifies baseline viral mutants associated with treatment response to pegylated interferon in HBeAg-positive chronic hepatitis B.
Abstract: No significant difference between groups was found regarding C1653T and G1896A mutants.
Locus 5p13.1 may be associated with the selection of cancer-related HBV core promoter mutations.
PMID: 31341412
2019
International journal of medical sciences
Introduction: The precore mutation (G1896A), mutations in enhancer II (C1653T) and the BCP (T1753V and the double mutations, A1762T, G1764A), and deletions in the pre-S region have been reported to be associated with the development of HCC.
Nearly half of Ultrio plus NAT non-discriminated reactive blood donors were identified as occult HBV infection in South China.
Result: T/G1727A with G1896A and T/G1727C with G1896A were presented in OBI100/OBI228 and OBI74/OBI185, respectively.
Result: The ATG start codon was abolished by a point mutation (ntA1814C/T) in three cases; and the ntG1896A mutation introducing a stop signal was present in 10 (27.8%) sequences.
HBV mutation literature information.
PMID: 
2019
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