Discussion: Most of the clones from the sera samples taken in the 11th month of ADV therapy revealed the presence of the rtL80V mutation in the clonal analysis of the HBV variants.
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
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).
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,
[Genotype distribution of chronic hepatitis B and hepatitis C patients and investigation of the resistance patterns in hepatitis B cases].
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%).
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 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%
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: 19041149
2009
Journal of hepatology
Abstract: rtM204V clusters with mutations localized in the RT-B domain (rtV173L, rtL180M, and rtT184A/S) (bootstrap=0.94), while rtM204I clusters with mutations localized in the RT-A domain (rtS53N, rtT54Y, and rtL80I/V) (bootstrap=0.96) (without associations with HBsAg specific mutations).
[Mutations of HBV polymerase gene sequence in lamivudine-resistant chronic hepatitis B patients].
Abstract: Other resistant substitutions included rtL80V/I, rtT184S, and rtA200V, and combined mutation of triple resistant substitutions was detected in HBV RT region of 5 patients by direct sequencing.
HBV mutation literature information.
PMID: 
2010
Hepatitis monthly
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