Abstract: Among the 10 well-characterized N(t)RTI-resistance mutations, L80I/V, V173L, L180M, A181T, T184S, S202G and M204I/V were significantly associated with treatment with lamivudine, an l-nucleoside analog, and A181S/T/V and N236T were significantly associated with treatment with adefovir, an acyclic nucleoside phosphonate.
Result: Supporting these associations were the findings that each of the viruses with L82M or A200V had one or more established L-nucleoside mutation (L180M and/or M204IV) and that each of the viruses with
Hepatitis B genotype G and high frequency of lamivudine-resistance mutations among human immunodeficiency virus/hepatitis B virus co-infected patients in Brazil.
PMID: 20944991
2010
Memorias do Instituto Oswaldo Cruz
Abstract: In 10 patients with viremia, LAM-resistance mutations in the polymerase gene (rtL180M + rtM204V and rtV173L + rtL180M + rtM204V) were found, accompanied by changes in the envelope gene (sI195M, sW196L and sI195M/sE164D).
Th1 and Th2 immune response in chronic hepatitis B patients during a long-term treatment with adefovir dipivoxil.
Method: In brief, serum HBV DNA was amplified by PCR and pyrosequenced to detect the following mutations of HBV polymerase: I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T, S202G/I, M204V/I, N236T, and M250V.
Result: The serum samples of these two patients were examined for ten HBV mutations (I169T, V173L, L180M, A181V/T, T184G/S/A/C, A194T
Profile of HBV antiviral resistance mutations with distinct evolutionary pathways against nucleoside/nucleotide analogue treatment among Chinese chronic hepatitis B patients.
Abstract: rtM204 mutations (27 rtM204I, 15 rtM204V and 5 rtM204I/V cases) were detected at the highest frequency among 65 mutants (72.30% [47/65]) and found to display 16 combination mutation patterns, in which rtM204I and rtM204V were significantly associated with rtL80I/V and rtL180M, respectively (P<0.01).
Multidrug-resistant hepatitis B virus strain in a chronic Turkish patient.
Abstract: In the 18th month of the ETV monotherapy, direct sequencing showed reduced susceptibility to ETV (rtL180M+rtM204V).
Table: L180M
Discussion: Hence, all of the methods applied in this study are sufficient to establish that the rtM204V + rtV173L + rtL180M mutations are in the same genome and predominate.
Discussion: However, clonal analysis of the HBV variants revealed that the rtM204V + rtV173L + rt
Dynamics of hepatitis B virus resistance to entecavir in a nucleoside/nucleotide-naive patient.
Abstract: Entecavir-resistant quasi-species (rtM204V+/-rtL180M plus S202G) were found after week 112 and gradually became the predominant mutations afterwards.
Abstract: The lamivudine resistant quasi-species (rtM204V+/-rtL180M), absent at baseline, were emerged as early as 48 weeks after entecavir administration.
Telbivudine, a nucleoside analog inhibitor of HBV polymerase, has a different in vitro cross-resistance profile than the nucleotide analog inhibitors adefovir and tenofovir.
Abstract: Telbivudine was not active against HBV strains bearing lamivudine mutations L180M/M204V/I but remained active against the M204V single mutant in vitro, potentially explaining the difference in resistance profiles between telbivudine and lamivudine.
The profile of mutational clusters associated with lamivudine resistance can be constrained by HBV genotypes.
Abstract: rtM204V clusters with mutations localized in the RT-B domain (rtV173L, rtL180M, and rt Abstract: Covariate analysis showed that rtM204V clusters with rtL180M, rtL229V (corresponding to sF220L in the HBsAg), and, interestingly, with HBsAg mutation sS207N (bootstrap=0.95).
Spontaneous HBeAg seroconversion and loss of hepatitis B virus DNA after acute flare due to development of drug resistant mutants during entecavir monotherapy.
Abstract: Interestingly, a new mutant type with rtL180M+rtT184L was found alongside rtL180M+rtT184L+rtM204V/I at week 228 and appeared to develop independently, according to the sequence analysis.
Susceptibility of hepatitis B virus to lamivudine restored by resistance to adefovir.
Abstract: In both patients serial monotherapy caused the replacement in all HBV clones of wild-type virus by classical lamivudine resistant mutants (L180M and M204V/I), which were replaced subsequently by adefovir resistant mutants (A181V and N236T).
HBV mutation literature information.
PMID: 
2010
Antiviral research
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