Result: We purified Result: While L60V-HBc, WT-HBc and F97L-HBc had similar transition temperatures between 91 C and 95 C, the transition temperature of P5T-HBc was much lower (TM = 86 C), showing that the mutation P5T weakens the stability of the whole capsid substantially.
Result: While in WT-HBc and P5T-HBc, the phenylalanine side-chain of F97 pointed towards the dimer axis, in L60V-HBc, it had an additional alternate position pointing away from the dimer axis (Figure 3g).
Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97.
8Discussion: However, neither the mutants (P5T and L60V) nor wt HBc-CLPs with bound peptides show Phe-97 is in ""conformation 2"" suggesting that flipping of Phe-97 is disp
Result: Previous studies have shown that CLPs of both mutants are structurally almost indistinguishable from wt HBc with the exception that Phe-97 adopts both alternate rotamer conformations with similar occupancy in HBc-L60V.
Discussion: It is hard to reconcile how a pocket factor that is mimicked by TX100 could act as maturation signal considering that we do not see any major differences in the structural mode of binding in naturally occurring mutants (F97L, P5T and L60V) with different secretion phenotypes.
Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model.
3Introduction: Interestingly, while a single HBc mutation L60V or P5T displayed a low-level secretion phenotype, a single mutation P130T led to a ""hypermaturation phenotype"" characterized by an increased abundance of both intracellular and extracellular fully mature full-length RC DNA."
The L60V variation in hepatitis B virus core protein elicits new epitope-specific cytotoxic T lymphocytes and enhances viral replication.
Abstract: In this study, we identified the L60V variation in HBc that generates a new HLA-A2-restricted CD8(+) T cell epitope by screening an ov
Abstract: The HBc L60V variation is correlated with hepatic necroinflammation and higher viral levels, and it may be associated with a poor prognosis in CHB patients.
Abstract: Therefore, our work provides further dissection of the impact of the HBc L60V variation, which orchestrates HBV replication, viral persistence, and immunopathogenesis during chronic viral infection.
Abstract: These data suggest that the HBc L60V variation can impact both HBV replication and HBV-specific T cell responses.
Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon alpha.
Method: Using pCMV-HBc (WT), the other three plasmids [pCMV-HBc (L60V), pCMV-HBc (S87G) and pCMV-HBc (I97L)] expressing HBc proteins with the substitutions L60V, I97L and Method: pCMV-HBc (WT), pCMV-HBc (L60V), pCMV-HBc (S87G) and pCMV-HBc (I97L) were confirmed by sequencing and these vectors were able to express the HBc protein/Flag-tag fused protein.
[Study of the quasispecies dynamics of serum hepatitis B virus in a patient with acute exacerbations of chronic hepatitis B].
Abstract: Hot-spot mutations in hepatitis B virus core gene: eliciting or evading immune clearance? The biological implications of substitutions L60V and I97L in the core (c) gene of hepatitis B virus (HBV) were investigated in order to determine whether they could change the immunogenicity of HBcAg or influence the immune response in mice.
Abstract: In conclusion, the L60V and I97L substitutions had no influence on humoral immune responses, but could downregulate T-cell responses to HBcAg, suggesting that L60V and I97L were immune escape mutants.
Abstract: The biological implications of substitutions
[Relationship between the HBV core gene mutation and the cellular immunity in host].
Abstract: OBJECTIVES: To study the relationship between the mutation of Leu60Val in HBV core region and the cellular immunity in patients with chronic hepatitis B (CHB).
Abstract: RESULTS: The mutation of Leu60Val was found in 19 out of the 91 CHB patients.
HBV mutation literature information.
PMID: 
2022
Clinical and experimental hepatology
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