Distinctive HBV Replication Capacity and Susceptibility to Tenofovir Induced by a Polymerase Point Mutation in Hepatoma Cell Lines and Primary Human Hepatocytes.
PMID: 33562603
2021
International journal of molecular sciences
Discussion: Nevertheless, some recent studies have shown that rtS78T/sC69*, rtS106C/rtH126Y/rtD134E/rtL269I, and rtL180M/T184L/M204V/rtA200V are related to TDF resistance.
Investigation of immune escape-associated mutations of hepatitis B virus in patients harboring hepatitis B virus drug-resistance mutations.
PMID: 32994690
2020
World journal of gastroenterology
Introduction: A few drug-resistance mutations, such as rtS78T and rtA181T, introduce a stop codon in the overlapping S region and affect the immune response, thereby influencing the clinical presentation of NA-treated patients.
Hepatitis B virus mutation pattern rtL180M+A181C+M204V may contribute to entecavir resistance in clinical practice.
Introduction: Moreover, HBV rtL269I and rtS78 T/sC69stop mutations were respectively reported being associated with enhanced viral replication of LAMr mutants and insufficient response to ETV treatment.
Patterns of hepatitis B virus S gene escape mutants and reverse transcriptase mutations among genotype D isolates in Jordan.
Discussion: The sC69*, with the concomitant rtS78T mutation impaired viral replication in vitro, which may explain the association of sC69* with low HBV DNA levels in patient sera.
Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment.
Introduction: Virological breakthrough on TDF therapy has been reported in two patients harbouring rtS78T/sC69 mutations, and in another patient with multi-site polymerase mutations; rtL80M, rtL180M, rtM204V/I, rtA200V, rtF221Y, rtS223A, rtT184A/L, rtR153Q, and
Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis.
Result: One patient (Pt11) harbored novel emergent substitutions (rtH13S, rtS78T, and rtQ267R/M) without LVDr substitutions.
Result: Phenotypic analysis of recombinant clones from this patient harboring either rtS78T+rtQ267R or rtH13S+rtQ267M did not show reduced susceptibility to ETV (<=1.0-fold WT; Table 4), suggesting no impact on ETVr.
Table: S78T
Effects of amino acid substitutions in hepatitis B virus surface protein on virion secretion, antigenicity, HBsAg and viral DNA.
Result: Due to the overlapping nature of the S and RT gene regions, mutations in the S gene may result in concomitant mutations in RT, such as sC69*/rtS78T, s Result: The potential factors might include the altered RT activities of rtS78T/sC69* and rtR153Q/sG145R, the altered stabilities of mutant mRNAs, the replenishment efficacies of cccDNA pool and so on.