Introduction: However, in the presence of rtM204I/V mutations, ETV resistance arose with the coexistence of rtI169T, rtL180M, rtT184A/F/G/I/L/S, rtS202G/I, or rtM250V mutations.
Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B.
Introduction: However, in the presence of rtM204I/V mutations, ETV resistance can occur if the rtI169T, rtT184A/F/G/I/L/S, rtS202G/I, or rtM250V mutation coexists.
Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations.
Conclusion: Under the latter therapeutic scheme, only ephemerally and with minor contribution (~5%), the A181T and T184L lamivudine-adefovir and entecavir resistance-associated mutations were detected, respectively.
Table: T184L
Discussion: In spite of the fact that the A181T adefovir-resistance and the T184L entecavir-resistance mutations were present in the background, they were only minor components of the HBV quasispecies that emerged once tenofovir was added in two consecutive samples separated by a five-month interval.
[Efficacy and safety of lamivudine plus adefovir combination therapy and entecavir monotherapy for chronic hepatitis B patients].
Abstract: Four patients in monotherapy cohort were found with virological breakthrough at 96 weeks and three cases among were confirmed to be of variants associated with ETV resistance (rtL180M + T184L + M204V).
Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection.
Method: The rtT184A/C/F/G/I/L/M/S, rtS202C/G/I and rtM250I/L/V were defined as the signature ETV-resistant mutations (ETV-R) if concomitant with rtM204I/V.
Table: T184I/L
Table: T184L/A
Table: T184L
Mechanistic characterization and molecular modeling of hepatitis B virus polymerase resistance to entecavir.
Result: Among those that grew well, both large (T184L/M/F/Q/N) and small (T184A/G
Result: Several different ETVr substitutions have been observed in ETV-treated patients, including T184A/C/F/G/I/L/M/S, S202C/G/I, and M250 I/L/V.
Result: The larger substitution T184L forces the ETV binding pocket closed as the YMDD loop is repositioned to accommodate the larger amino acid.
Table: T184L
Discussion: The larger T184L and S202I substitutions are examples that sterically affect the YMDD loop position.
Mechanism of entecavir resistance of hepatitis B virus with viral breakthrough as determined by long-term clinical assessment and molecular docking simulation.
PMID: 19933798
2010
Antimicrobial agents and chemotherapy
Abstract: Modeling of HBV reverse transcriptase (RT) by docking simulation indicated that a combination of LVDr and ETVr (T184L or S202G) was characterized by a change in the direction of the D205 residue and steric conflict in the binding pocket of ETV triphosphate (ETV-TP), by significantly longer minimal distances (2.2 A and 2.1 A), and by higher potential energy (-117 and -99.8 Kcal/mol) for ETV-TP compared with the wild type (1.3 A; -178 Kcal/mol) and LVDr substitutions (1.5 A; -141 Kcal/mol).
Abstract: Our data suggest that the low binding affinity of ETV-TP for the HBV RT, involving conformational change of the binding pocket of HBV RT by L180M, M204V plus T184L, and
Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients.
PMID: 19301976
2009
The Journal of infectious diseases
Method: Established NRTI-resistance mutations included the following RT mutations: rtL80V/I, rtI169T, rtV173L, rtL180M, rtA181TV, rtT184S/A/I/L/F/G, rtA194T, rtS202G/I, rtM204V/I/S, rtN236T, and rt PMID: 19302908
2009
Clinical therapeutics
Abstract: A total of 9.1% (4/44) of the clones harbored the rtL180M + rtT184L + rtM204I mutations.
Abstract: At week 22 during ADV treatment, LAM-resistance mutations (rtL180M, rtT184L, rtM204I, rtV191I, and rtL229V) were not detected.
Abstract: The rtM204I mutation was associated with compensatory mutations (rt
Evolution of hepatitis B virus mutation during entecavir rescue therapy in patients with antiviral resistance to lamivudine and adefovir.
HBV mutation literature information.
PMID: 
2012
Hepatitis monthly
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