Discussion: This result is consistent with a previous study demonstrating that the HBx with A1762T/G1764A (K130M/V131I) mutation (the same as M1-HBx in our study) had a stronger tumorigenic effect than its WT counterpart in a SB mouse model.
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.
Discussion: In rt269I signature NS mutations, several types, including preC-W28Stop (1896 preC mutation) and two types in the X region, V/L5M and V131I, are strongly related to HBeAg seronegative infections, which can lead to enhanced persistent rt269I type HBV infections by increasing mutation frequencies within the HBV genome, particularly in the Pol region, perhaps because of a host immune response.
Discussion: Indeed, we found several rt269I signature mutation types related to lower HBV replication (I84T/M
Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants.
Discussion: The A1762T/G1764A mutations are responsible for the K130M/V131I mutations found in the HBx.
Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients.
Abstract: Multinomial regression analysis revealed that the K130M/V131I mutations were correlated with CLD progression (OR, 7.629; 95% CI, 1.578-36.884).
Abstract: Significant differences in viral load were found in HBV-infected patients who had X gene mutations, such as R87W/G, I127L/T/N/S and K130M/V131I mutations (P<0.05).
Abstract: The presence of K130M and V131I mutations may be predictive for the progression of HBV-associated CLD in Indonesia.
Result: Multinomial regression analysis confirmed that K130M/V131I mutati
Association Between HBx Variations and Development of Severe Liver Disease Among Indonesian Patients.
PMID: 31341154
2019
The Kobe journal of medical sciences
Abstract: In addition, the double mutation K130M/V131I and the triple mutation N88V/K130M/V131I were associated with a 2.5 times higher risk of advanced liver disease.
HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism.
Abstract: IMPLICATIONS: Our findings suggested that HBx-K130M/V131I-mutant variant promoted HCC progression by activating AKT/FOXO1 pathway and inducing stronger inflammation in liver via AA metabolism.
Abstract: Taken together, the increased rate of HCC observed in chronic hepatitis B patients with K130M/V131I-mutated X protein, may be due to changes in AA metabolism and AKT/FOXO1 signaling.
Abstract: To compare the potential tumorigenic effects of K130M/V131I (Mut) and wild-type (WT) HBx on PMID: 32003338
2019
Indian journal of medical microbiology
Abstract: The frequency of aminoacid substitution in proapoptotic domain was higher in HBeAg negative participants including I127V (34%), K130M (34%), V131I (40%).
Abstract: The frequency of double mutation (K130M+V131I) and triple mutation (I127V+K130M+V131I) were found to be higher (32% and 36%) in HBeAg negative participants.
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
Introduction: Mutations within the X gene, including V5M, I127T, K130M, and V131I/L, are risk factors for HCC and may promote the progression of liver degradation (Kim et al.,).
Hepatitis B virus (HBV) X gene mutations and their association with liver disease progression in HBV-infected patients.
Abstract: I127T, V131I, and F132Y/I/R mutations showed a significant increasing trend associated with the disease progression to HCC.
Abstract: One double mutation (K130M+V131I) and two triple mutations (I127T+K130M+V131L and K130M+V131I+F132Y) were observed, with significant rising prevalence through progressive clinical phases of liver disease to HCC.
Introduction: In addition, K130M+
HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism.
Abstract: Hepatitis B virus (HBV) genomic mutations A1762T, G1764A and AG1762/1764TA cause production of HBV X protein (HBx) mutants, namely K130M, V131I and KV130/131MI.
HBV mutation literature information.
PMID: 
2022
Frontiers in oncology
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