Genotypic resistance profile of hepatitis B virus (HBV) in a large cohort of nucleos(t)ide analogue-experienced Chinese patients with chronic HBV infection.
Result: By contrast, rtM204I was more often accompanied by rtL80I (36.5%) than rtM204V (3.9%).
Discussion: Amongst these, rtL80I was reported to compensate for the loss of replication efficiency associated with the acquisition of LAM resistance, particularly in the case of rtM204I [45].
Discussion: Our results were consistent with this view as 85.2% of rtL80I concurred with rtM204I and rtM204I/V.
Discussion: T
Acute hepatitis B infection associated with drug-resistant hepatitis B virus.
Abstract: RESULTS: Direct PCR sequencing showed that 14 samples (7.0%) were positive for drug-resistant HBV variants, comprised of 11 with the lamivudine-resistant pattern rtM204I and/or rtM204V in the presence and absence of compensatory mutations rtL80I, rtV173L, and rtL180M; two with the adefovir-resistant pattern rtA181V; and one with the entecavir-resistant pattern rtL180M+rtS202G+rt
Response to adefovir depends on mutation patterns in precore region, basal core promoter and reverse transcriptase, and on-treatment responses in Lamivudine-resistant chronic hepatitis B patients.
Abstract: PC mutation, the absence of compensatory mutations (rtL80I/V or rtV173L), and a decrease in serum hepatitis B virus (HBV) DNA by 3 log or greater at 6 months were independent predictors of virologic response.
Hepatitis B virus drug resistance in HIV-1-infected patients taking lamivudine-containing antiretroviral therapy.
Abstract: All 19 patients with HBV-DR had lamivudine resistance with the mutations as follows: M204V/I (95%), L180M/A181T (95%), L80V/I (47%), V173L (32%), and N236T (21%).
[Resistance mutation patterns of hepatitis B virus in patients with suboptimal response to adefovir dipivoxil therapy after lamivudine resistance].
Abstract: 20% of clones from three serum samples were detected double resistance to LAM and entecavir (ETV) in the combination therapy group, the resistance patterns were M204I+L80I+T184I (2/10), M204V+L180M+T184S (2/10), and M204V+L180M+G173L+S202G (2/10) respectively.
Abstract: CONCLUSIONS: In the patients with suboptimal viral response to ADV therapy after LAM resistance, the ADV resistance mutation patterns of A181T+N236T, A181V and A181T could easily be selected during ADV monotherapy; while in th
Hepatitis B virus reverse transcriptase sequence variant database for sequence analysis and mutation discovery.
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: Twelve mutations at the eight of these 10 positions were significantly associated with N(t)RTI therapy (Fisher's Exact test; Benjamini-Hochberg adjusted p value <0.01): L80I/V, V173L, L180M,
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.
Discussion: On the other hand, compensatory mutations such as rtV173L, rtQ215H, and rtL80I/V have been detected only by direct sequencing and LIPA, respectively.
Discussion: Some compensatory mutations demonstrated in this study (rtL80I/V, rtV173L, rtL180M, rtQ215H) help to restore the replication efficiency of the mutant virus, but they tend to occur in the presence of antiviral selection pressure.
[Long-term clevudine therapy in nucleos(t)ide-naive and lamivudine-experienced patients with hepatitis B virus-related chronic liver diseases].
PMID: 19581770
2009
The Korean journal of hepatology
Abstract: Proven sites of mutation of HBV DNA polymerase in naive patients were, for example, L80I, L180M, A181V/T, M204I and V207I.
Hepatitis B virus with the rtL80V/I mutation is associated with a poor response to adefovir dipivoxil therapy.
Abstract: CONCLUSIONS: These results provide evidence that rtL80V/I variants of HBV may be associated with a poor antiviral response to ADV in CHB patients with YMDD mutants.
Abstract: However, interestingly, after ADV therapy for 12 months, patients with rtL80V/I achieved a much smaller reduction in serum HBV-DNA titre than those without it (mean, -3.43 vs.
Abstract: In addition, patients with rtL80V/I had lower rates of undetectable HBV-DNA (20 vs.
Abstract: The rtL80V/I and rtL180M variants were identified in 66 (68%
HBV mutation literature information.
PMID: 
2011
Journal of viral hepatitis
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