Discussion: Single mutants in the YMDD motif (rtM204V/I) replicate substantially more slowly in vitro than the wild type.
Discussion: The resistance occurs by replacement of a methionine residue at position rt204 by either valine (rtM204V) or isoleucine (rtM204I), accompanied or not by a substitution at position rt180 and more rarely by a substitution at position rt173.
Discussion: The triple mutation rtV173L/rtL180M/ PMID: 18329126
2008
Journal of hepatology
Abstract: The M204V/I mutation was detected in 43% (15/35) and 15% (6/41) of each group, respectively.
Impact of hepatitis B virus rtA181V/T mutants on hepatitis B treatment failure.
Abstract: RESULTS: Clonal analysis revealed the co-localization on the same HBV genome of rtA181T/V with rtN236T, but not with rtM204V/I mutations following lamivudine, adefovir or lamivudine+adefovir breakthrough.
[Mutations of HBV polymerase gene sequence in lamivudine-resistant chronic hepatitis B patients].
Abstract: RESULTS: Lamivudine resistant mutation was detected in 103 patients, and the major mutations included rtL180M+rtM204V and rtM204I, accounting for 58.3% and 22.3%, respectively.
[A five-year analysis of HBV mutations in a multidrug-resistant patient with chronic hepatitis B].
Abstract: RESULTS: Several mutations were identified in succession, including LAM-resistant mutations M204I/V and L180M+M204V, ETV-resistant mutation S202G, and HBeAg nonsense mutation G1896A.
Supportive role played by precore and preS2 genomic changes in the establishment of lamivudine-resistant hepatitis B virus.
PMID: 18713056
2008
The Journal of infectious diseases
Abstract: BACKGROUND: Hepatitis B virus (HBV) establishes lamivudine resistance via the resistance-causative rtM204V/I mutation and the replication-compensatory rtL180M mutation.
Understanding the molecular basis of HBV drug resistance by molecular modeling.
Abstract: In this regard, homology modeled structure of HBV-polymerase was used for minimization, conformational search and induced fit docking followed by binding energy calculation on wild-type as well as on mutant HBV-polymerases (L180M, M204V, M204I, L180M+M204V, L180M-M204I).
Result: A further binding mode study reveals a steric clash in case of M204I HBV due to the unfavorable position and orientation of a methyl group (Figure 13b) of I204 residue.
Result: Energetic results in Table 4 clearly indicates a significant low binding affinity of 3TC-TP (DeltaE = -346.7 KJ/mol) in comparison to dCTP (DeltaE = -426.5 KJ/mol) in
[Multiple-site analysis of HBV drug-resistant mutations in 340 patients with chronic hepatitis B].
Abstract: M204V and M204I were the most common LAM-resistant mutations.
Abstract: LdT-resistance was observed as M204I.
[Development of clevudine resistance after switching from lamivudine in a patient with chronic hepatitis B].
PMID: 19077481
2008
The Korean journal of gastroenterology
Abstract: After the 6 months of clevudine therapy, the patient developed virologic breakthrough (>1.0chi10(8) copies/mL) as well as biochemical breakthrough, which was associated with the presence of rtM204I plus rtL80I mutant.
Primary resistance, multidrug resistance, and cross-resistance pathways in HBV as a consequence of treatment failure.
Abstract: Several major HBV-evolutionary NA-resistance pathways (rtM204I/V, rtN236T and rtA181T/V) have now been characterised.
Abstract: The rtM204V/I pathway is responsible for resistance to the L: -nucleosides, such as lamivudine (LMV), telbivudine (LdT) and clevudine (CLD), and also entecavir (ETV), whilst the rtN236T pathway is responsible for adefovir (ADV) and tenofovir (TFV) resistance.
HBV mutation literature information.
PMID: 
2008
BMC microbiology
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