1Abstract: The peptide ""GSLLGRMKGA"" binds weakly to hepatitis B core protein capsids and mutant capsids with a premature (F97L) or low-secretion phenotype (L60V and P5T)."
Method: For the model building of P5T-HBc, L60V-HBc and P1/P2 bound to WT-HBc, P5T-HBc, F97L-HBc and L60V-HBc, the pdb model 6HTX was modified and fit into EM maps.
Method: For this, the current model of the asymmetric unit o
Binding of a Pocket Factor to Hepatitis B Virus Capsids Changes the Rotamer Conformation of Phenylalanine 97.
Abstract: Similar changes occur in mutants with low secretion phenotypes (P5T and L60V) and in a mutant with a pre-mature secretion phenotype (F97L).
Introduction: Naturally occurring point mutations like HBc-F/I97L with an immature secretion phenotype or point mutations with a low secretion phenotype, such as HBc-L60V and HBc-P5T, are located in the area surrounding the pocket.
Introduction: We asked what the underlying conformational changes were and whether these changes differed between CLPs of wt HBc, mutants with immature secretion phenotype (HBc-F97L) or mutants wi
A nuanced role of the small loop of hepatitis B virus small envelope protein in virion morphogenesis and secretion.
8Discussion: Naturally occurring core mutants I97L (isoleucine to leucine) or F97L (phenylalanine to leucine), exhibited a so-called ""immature secretion"" phenotype, which allows excessive secretion of virions containing an immature genome."
Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate.
Introduction: Previous studies have shown that the substitution of proline (P) with threonine (T) at codon 5 of HBcAg caused lower levels of virion secretion, which, would revert to the wild type secretion phenotype when it coexisted with F97L mutation.
Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model.
Introduction: In addition to the trans-defect in virion secretion, a cis-defect in intracellular viral DNA synthesis was also detected in mutant F97L by a genetic complementation assay.
Introduction: Recently, in another cryoEM study, this pocket in the mutant F97L virions was found enlarged.
Introduction: Using a cis-trans genetic test design, we demonstrated that it is the trans-acting mutant F97L HBc protein, rather than the mutant F97L pgRNA, that is responsible for the extracellular immature virion secretion.
Introduction: While HBc mutant I97L is frequent in the genotype C (serotype adr), mutant F97L is common in the genotype D (serotype ayw) (; see also references cited in reference).
R
Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma.
8Discussion: Interestingly, the most frequently observed naturally occurring core protein mutation found in CHB and also in HCC patients I97L or F97L which is associated with ""immature virion secretion"" was completely absent in Indian patients with HBV-genotype D while among the ""low secretion core variants"" such as P5T/A/S, a new variant P5R was noted with high frequency in HBV-genotype D related HCC in previous Indian study."
Chimeric constructs between two hepatitis B virus genomes confirm transcriptional impact of core promoter mutations and reveal multiple effects of core gene mutations.
Abstract: Since the structures of the mutant and wild-type capsids are essentially the same and the mutation is not involved in the contact between dimers, we suggest that the F97L mutation affects the dynamic behavior of dimer and capsid.
Abstract: We examined in vitro assembly of empty HBV capsids from wild-type and F97L core protein assembly domains.
Influence of a putative intermolecular interaction between core and the pre-S1 domain of the large envelope protein on hepatitis B virus secretion.
Abstract: In addition, the secretion kinetics of the mature genomes are comparable between the wild-type HBV and the mutant F97L.
Abstract: In this study, our kinetic analysis of virion secretion of the mutant F97L (phenylalanine to leucine) indicates that the secretion of its immature genome does not occur earlier than that of its mature genome.
Abstract: Therefore, the immature secretion phenomenon of mutant F97L is not caused by premature secretion or more efficient secretion.
The mechanism of an immature secretion phenotype of a highly frequent naturally occurring missense mutation at codon 97 of human hepatitis B virus core antigen.