HBV mutation literature information.


  Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan.
 PMID: 30867996       2019       PeerJ
Abstract: RT mutations included: V173L, S202I, L180M, M204V and T184A.
Abstract: These mutations included: L109R, Q129R, M133L, S143L and D144E with overall prevalence of 18.9%
Introduction: Among other commonly detected vaccine-escape mutants are: P120Q, Q129H, F134Y/L, S143L and D144A/E.
Introduction: The prototypic and most stable vaccine-escape mutant is G145R.


  A nonsense mutant of the hepatitis B virus large S protein antagonizes multiple tumor suppressor pathways through c-Jun activation domain-binding protein1.
 PMID: 30870427       2019       PloS one
Discuss
Discussion: Although the in vivo transfection by hydrodynamic injection showed a relatively strong and prolonged expression of the LHBs sW182* protein in the mouse liver, this method is considered as transient transfection with a limited efficiency (only part of the liver cells are transfected).
Discussion: Because of the labile nature of the mutant in the cultured liver cells, we only transiently expressed the sW182* in Huh-7 cells, which showed a low, but reasonable amount of the protein expression (Fig 1).
Discussion: Consistently, depletion of Jab1 from the liver cells impaired the effect of the LHBs sW182* to downregulate the tumor suppressors and their target genes (Figs 4 and 5).


  Molecular cloning and phenotypic analysis of drug-resistance mutants with relevant S-region variants of HBV for a patient during 189-month anti-HBV treatment.
 PMID: 30882363       2019       Antiviral therapy
Abstract: Interestingly, the rtA181T-causative sW172stop to sW172non-stop mutation transition was observed at HBV DNA fluctuations.


  Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate.
 PMID: 30902704       2019       Antiviral research
Abstract: Further mutagenesis study revealed that the P5T mutation of core protein plays an important role in the enhanced viral replication through increasing the levels of capsid formation and pregenomic RNA encapsidation.
Method: The core gene point mutations (P5T, S35T, S87G, I97L, Q177K) and the reversion mutations (T5P, T35S, Q79P, D83E, G87S, L97I, K177Q) were individually introduced into pCMVHBV-WT and pCMVHBV-GYF, respectively, by us


  Viral quasispecies of hepatitis B virus in patients with YMDD mutation and lamivudine resistance may not predict the efficacy of lamivudine/adefovir rescue therapy.
 PMID: 30906435       2019       Experimental and therapeutic medicine
Abstract: Furthermore, although in the non-responder group the frequency of the LAM resistance-associated mutations (rtM204V/I) decreased at 6 months compared with the baseline, it did not disappear in any of the patients after six months of treat
Introduction: ADV-resistance has been associated with the rtN236T mutation in the D domain and/or the rtA181V/T mutation in the B domain.
Introduction: It has been indicated that LAM resistance is mostly associated with the rtM204I/V mutation in the tyrosine-methionine-aspartate-aspartate (YMDD) motif of the C domain of the polymerase gene.


  Molecular and serological characterization of occult hepatitis B virus infection among patients with hemophilia.
 PMID: 30908666       2019       Journal of medical virology
Abstract: sR73H, sI110L, sP120A, sP127T, sQ129H, sG130R, and sC137S were shown to be the most determinant escape mutation and OBI-relevant mutants.


  Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors.
 PMID: 30943997       2019       Virology journal
Abstract: Sequencing revealed multiple substitutions in preS1, preS2, and S regions for one panel including a rare D144N substitution associated with vaccine breakthrough that emerged with increasing frequency as the breakthrough infection developed.
Figure: The bars above the 6272 graph show the percentage of codons with the HBsAg D144N mutation.
Discussion: Hydrophilicity analysis of the second loop of the HBsAg major hydrophilic region by the Hopp & Woods method indicated that a mutation to asparagine at amino acid 144 would result in a reduction in hydrophilicity similar to that for the A/H mutations, suggesting that the D144N mutation may affect the presentation or conformation of this epito


  HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism.
 PMID: 30975706       2019       Molecular cancer research
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: 31046787       2019       Virology journal
Discussion: Another limitation of the study was our failure to clarify whether HBV with the G2765A substitution is actually less infectious to hepatocytes, and we could not directly show whether the mutation is associated with a decrease in the L/S protein ratio in patient sera due to technical reasons.
Discussion: In fact, G2765A mutant HBV-infected patients showed less severe disease.
Discussion: In fact, the aminotransferase levels of patients infected with the G2765A mutant HBV tend to be low, indicating that the immune responses of those patients are weak.
Discussion: Our data from the clinical samples showed that the G2765A substitution was associated with a lower HBV DNA load.


  Analysis of hepatitis B virus genotype and gene mutation in patients with advanced liver disease in East Kalimantan, Indonesia.
 PMID: 31086664       2019       Biomedical reports
Abstract: The C1505A mutation in X region, T1753V and A1762T/G1764A mutations in the basal core promoter region and C1858T in precore (PC) region were frequent and only detected in patients with ALD (28.9, 40, 73.5 and 17.6%, respectively), whereas the G1896A mutation in the PC region was frequently detected in HBV carriers.



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