A study on sequence variations in pre-S/surface, X and enhancer II/core promoter/precore regions of occult hepatitis B virus in non-B, non-C hepatocellular carcinoma patients in Taiwan.
PMID: 19431214
2009
International journal of cancer
Abstract: Compared with the HBsAg-positive HCC controls, occult HBV-infected HCC patients had higher frequencies of M1I and Q2K in pre-S2 gene, G185R and S210N in surface gene, A36T and A44L in X gene, and G1721A in enhancer II gene, and had lower rates of pre-S deletions and A1762T/G1764A, PMID: 19456899
2009
Hepatology research
Abstract: RESULTS: Higher HBV DNA levels, subgenotype B1/Bj, A1762T/G1764A, G1896A, G1899A and A2339G mutation were significantly more frequent (P < 0.05), while hepatitis B e-antigen was less frequent in the FH-T patients than AHB.
Genotype-specific genomic markers associated with primary hepatomas, based on complete genomic sequencing of hepatitis B virus.
Abstract: HCC-related mutations T31C, T53C, and A1499G were associated with HBV subgenotype Ce, and mutations G1613A, G1899A, T2170C/G, and T2441C were associated with HBV subgenotype Cs.
Effect of basal core promoter and pre-core mutations on hepatitis B virus replication.
PMID: 18343830
2008
The Journal of general virology
Abstract: Substitutions A1762T/G1764A and T1753C, C1766T and T1768A in the BCP region, and G1896A and G1899A in the pre-C region, were examined either alone or in combination, using a common genetic background.
Abstract: The double BCP mutation (A1762T/G1764A) and the pre-C mutations (G1896A, G1899A), either alone or in combination, had no appreciable effect on the replication capacity of the virus.
Clinical significance of basal core promoter and precore mutations in chronic hepatitis B.
Abstract: HBeAg-negative samples were associated with precore mutations (G1896A and G1899A).
Hepatitis B virus genotype E detected in Brazil in an African patient who is a frequent traveler.
PMID: 17934636
2007
Brazilian journal of medical and biological research
Abstract: The preC/C region showed G1896A and G1899A mutations but no mutations in the basal core promoter.
Initial load of hepatitis B virus (HBV), its changing profile, and precore/core promoter mutations correlate with the severity and outcome of acute HBV infection.
Abstract: In univariate analysis, seronegativity for hepatitis B envelope antigen (HBeAg) and mutations in both the precore (G1896A and/or G1899A) and core promoter (T1753A/C and/or T1754C/G and/or A1762T/G1764A) were associated with FH (odds ratio [OR], 5.60; P=0.0269 and OR, 52.0; P=0.0006; respectively).
Sequential accumulation of the basal core promoter and the precore mutations in the progression of hepatitis B virus-related chronic liver disease.
Abstract: The T to C/A mutation at nucleotide 1753 in the BCP and G to A mutation at nucleotide 1899 in the precore were more frequent in liver cirrhosis than in the other clinical statuses (p < 0.05).
Point mutations upstream of hepatitis B virus core gene affect DNA replication at the step of core protein expression.
Abstract: This replication defect was associated with reduced expression of core protein and could be overcome by a G1899A covariation, or by nonsense or frameshift mutation in the precore region.
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.
HBV mutation literature information.
PMID: 
2009
International journal of cancer
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