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*
Conclusion: Furthermore, more than half of the HBV-infected subjects harbored the stop codon W28* of the precore region that is responsible for the HBeAg negative state.
Introduction: The HBeAgphenotype arises due to some substitutions and more particularly a stop codon W28* in the precore sequence which is associated with abrogation of expression in the HBeAg level .
Result: The stop codon of W28* was detected in 55% (40/73) of the patients, which was the most frequent change in the precore sequence, but the difference among the groups was not significant (p = 0.69).
rt269I Type of Hepatitis B Virus (HBV) Polymerase versus rt269L Is More Prone to Mutations within HBV Genome in Chronic Patients Infected with Genotype C2: Evidence from Analysis of Full HBV Genotype C2 Genome.
Abstract: We also found that there are a total of 19 signature single nucleotide polymorphisms (SNPs), of which 2 and 17 nonsynonymous mutation types were specific to rt269L and rt269I, respectively: Of these, most are HBeAg negative infections (preC-W28*, X-V5M and V131I), lowered HBV DNA or virion production (C-I97F/L, rtM204I/V) or preexisting nucleot(s)ide analog resistance (NAr) (rtN139K/H, rtM204I/V and
[Effect of hepatitis B virus preC/C and S gene antigen epitope mutations on HBeAg serological status in patients with chronic hepatitis B].
Abstract: After adjusting for confounding factors such as age, gender, HBV genotype, serum alanine aminotransferase level and precw28 * mutations in the longitudinal studies, the results showed that TC cell epitope (prec47-56, prec117-125, s208-216) and Th cell epitope (prec176-185) were the main independent risk factors affecting the host HBeAg serological status.
Hepatitis B virus drug resistance mutations in HIV/HBV co-infected children in Windhoek, Namibia.
Result: Pre-C genomic changes were found in three samples: G1862T in sample 2C, and mixed populations of stop codon G1896A mutant and wild-type virus (W28*W) in samples 3C and 6C.
Discussion: The Pre-C stop codon G1896A (W28*) mutation, observed in two children, interrupts HBeAg production.
Discussion: The presence of both W28* and wild-type virus (W28*W) explained the HBeAg positive status noted in these two patients.
High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank.
Method: First, we classified 340 genotype C1 strains and 24 Cambodian isolates into 48 patterns by combinations of the following mutations pre-S deletion, G1613A, C1653T, T1753V, and A1762T/G1764A, Pre-C W28 stop codon, and P130 in the core region.
Result: Based on the presence or absence of the mutations of pre-S deletion, G1613A, C1653T, T1753V, A1762T/G1764A, Pre-C W28
Low incidence of precore W28* mutant variants in treated hepatitis B virus and human immunodeficiency virus co-infected patients.
Abstract: At baseline, 47 of 162 (29.0%) patients had the pcW28* mutation and were more frequently HBeAg-negative (adjusted-OR = 4.37, 95%CI = 1.76-10.86) and had non-A HBV genotypes (adjusted-OR = 9.14, 95%CI = 4.05-20.66).
Abstract: In 114 patients without baseline mutation and available data, four developed incident pcW28* mutation by the end of follow-up (cumulative 3.5%, 95%CI = 1.3-9.1%).
Abstract: In a three-year prospective cohort of 165 HIV-HBV co-infected patients, p
Abstract: In conclusion, the pcW28* mutation infrequently appeared in this co-infected study population with increased use of potent antivirals and suppressed levels of circulating virus.
The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease.
PMID: 30406036
2018
Frontiers in cellular and infection microbiology
Abstract: Two precore mutations, W28* and G29D, and six core mutations, F24Y, E64D, E77Q, A80I/T/V, L116I, and
Discussion: In the present study, we observed a statistically significant increase in preC-W28* frequency in the LC+HCC group of patients as compared with active HBV carriers, which is consistent with previous reports of a positive association between this mutation and liver disease severity (Kim et al.,; Park et al.,; Xie et al.,).
Novel HBV mutations and their value in predicting efficacy of conventional interferon.
PMID: 28381384
2017
Hepatobiliary & pancreatic diseases international
Abstract: PC-W28STOP (ntG1896A) was significantly higher in the combined response (CR) group than that in the no CR group (91.7% vs 39.7%, P=0.001).
Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients.
Result: besides classical A1762T/G1764A and G1896A mutants affecting codons 130/131 of X gene (K130M/V131I) and codon 28 of PC gene (W28stop), another 12 SNPs (nt.1719, nt.1726, nt.1727, nt.1730, nt.1752, nt.1753, nt.1768, nt.1800, nt.1803, nt.1804, nt.1805 and nt.1825) also caused amino acid changes.
Naturally occurring precore/core region mutations of hepatitis B virus genotype C related to hepatocellular carcinoma.
Result: Five mutations in the C region (C-D32N/H, C-E43K, C-P50A/H/Y, C-A131G/N/P and C-S181H/P) and two in preC (preC-W28* and preC-G29D) were found to affect the HBeAg serostatus.
Discussion: However, no variant of those five related to the HBeAg-negative serostatus was significantly related to