Association of Hepatitis B Virus Mutations of A1846T and C1913A/G With Acute-on-Chronic Liver Failure Development From Different Underlying Chronic Liver Diseases.
Result: In addition, since BCP/PC mutations of T1754G, T1758C, C1766T, T1768A, G1862T, and T1858C were observed only in 7, 5, 7, 4, 1, and 4 of ACLF patients, respectively, these mutations were not included in further analysis.
Variability of the preC/C region of hepatitis B virus genotype A from a South African cohort predominantly infected with HIV.
Discussion: A G1862T nucleotide mutation, which was identified in two study sequences (4070 and 4312) has also been reported to negatively affect HBeAg expression at post-translational level, however, both these participants were HBeAg-positive.
Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively.
PMID: 23903686
2013
Brazilian journal of medical and biological research
Abstract: Four patterns (C1810T, A1846T, G1862T, and G1896A) were significantly associated with HCC compared with LC.
Abstract: Multivariate regression analyses showed that HBV subgenotype C2 and C2-associated mutation patterns (C1653T, T1753C, A1762T, and G1764A) were independent risk factors for LC when CHB was the control, and that B2-associated mutation patterns (C1810T, A1846T, G1862T,
Molecular characterization of hepatitis B virus in liver disease patients and asymptomatic carriers of the virus in Sudan.
Introduction: 2009 found that G1862T has no effect on HBeAg expression.
Introduction: G1899A mutations increased DNA replication but the double mutation G1899A/G1862T was associated with considerably more replication compared to G1862T alone.
Introduction: G1862T and G1896A Mutations.
Introduction: G1862T was also implicated in reducing DNA replication severely.
Introduction: Among 52 FH patients, G1862T was detected in 7 patients (Table 3).
Introduction: In a study of in vitro translation, G1862T mutation ab
HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China.
PMID: 23304671
2012
Iranian journal of public health
Introduction: HBV mutations were often observed in the pre-C and basal core promoter (BCP) regions, such as T1753C, A1762T, G1764A, G1862T, G1896A and G1899A nucleotide acid substitution.
Genotyping and molecular characterization of hepatitis B virus from human immunodeficiency virus-infected individuals in southern Africa.
Abstract: Mutations affecting HBeAg expression at the transcriptional (1762T1764A), translational (Kozak 1809-1812, initiation 1814-1816, G1896A with C1858T), or post translational levels (G1862T), were responsible for the high HBeAg-negativity observed.
Abstract: The G1862T mutation occurred only in subgenotype A1 isolates, which were found in one third (7/21) of HBsAg(-ve) participants, but in none of the 18 HBsAg(+ve) participants (p<0.05).
Result: The G1862T, which interferes with post-translational modification of the HBeAg-precursor and affects HBeAg expression occurred in isolates from 7
Genetic analysis of precore/core and partial pol genes in an unprecedented outbreak of fulminant hepatitis B in India.
Abstract: A1762T, G1764A basal core promoter (BCP) mutations, insertion of isoleucine after nt 1843, stop codon mutation G1896A, G1862T transversion plus seven other mutations in the core gene caused inhibition of HBeAg expression implicating them as circulating precore/BCP mutant virus.
Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B-related acute-on-chronic liver failure without pre-existing liver cirrhosis.
Introduction: In addition, single mutations including the T1753V (C/A/G), C1766T, T1768A, G1862T and G1899A in the BCP/PC region have been reported to be associated with increased HBV replication capacity and/or reduced HBeAg expression in vitro, and in some cases associated with ALF in the clinic.
Enhanced intracellular retention of a hepatitis B virus strain associated with fulminant hepatitis.
Abstract: The pBFH2 construct with A1762T/G1764A, G1862T, and G1896A showed the largest amount of core particle-associated intracellular HBV DNA, but no significant increase of extracellular HBV DNA in comparison with the wild construct, suggesting that these mutations might work together for retention of the replicative intermediates in the cells.