Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment.
Result: Functional consequences of rtS78T/sC69* and preS1/preS2del on viral replication and secretion.
Result: Our UDPS analysis revealed over-representation of the rtS78T mutation in the reverse transcriptase (rt) gene of the HBV genome that creates a premature stop codon in the overlapping surface (s) protein at sC69, thereby deleting almost the entire small HBV surface protein.
Result: Patient B showed 13.96% frequency for rtS78T
HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining.
Introduction: identified rtS78T as being partially responsible for multidrug resistance to ETV and TDF in two patients receiving ETV-TDF combination therapy.
Genotyping and Mutation Pattern in the Overlapping MHR Region of HBV Isolates in Southern Khorasan, Eastern Iran.
Discussion: The rare S78T mutation also observed in one patient can lead to tenofovir resistance.
Amino acid similarities and divergences in the small surface proteins of genotype C hepatitis B viruses between nucleos(t)ide analogue-naive and lamivudine-treated patients with chronic hepatitis B.
Abstract: Interestingly, another newly-identified truncation mutation sC69stop/rtS78T decreased from 7.91% (11/139) in NA-naive cohort to 2.70% (2/74) in LMV-treated one.
Anti-HBV treatment induces novel reverse transcriptase mutations with reflective effect on HBV S antigen.
Abstract: Indeed, rtS78T (prevalence: 1.1% in drug-naive and 12.2% in adefovir-failing patients) decreased the RT-affinity for adefovir more than the classical adefovir-resistance mutations rtA181 T/V (WT:-9.63 kcal/mol, rtA181T:-9.30 kcal/mol, rtA181V:-7.96 kcal/mol, rtS78T:-7.37 kcal/mol).
Abstract: RESULTS: Ten novel RT-mutations (rtN53T-rtS78T-rtS85F-
Clinical emergence of entecavir-resistant hepatitis B virus requires additional substitutions in virus already resistant to Lamivudine.
PMID: 15328117
2004
Antimicrobial agents and chemotherapy
Abstract: For liver transplant patient B (AI463015-B), previous famciclovir, ganciclovir, foscarnet, and 3TC therapies had failed, and RT changes rtS78S/T, rtV173L, rtL180M, rtT184S, and rtM204V were present at study entry.
HBV mutation literature information.
PMID: 
2017
Journal of hepatology
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