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: Against HBV genomes with known telbivudine-resistance mutations, M204I and L80I/M204I, telbivudine, lamivudine and entecavir lost 353- to >1000-fold activity whereas adefovir and tenofovir exhibited no more than 3-5-fold change.
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 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).
Association of lamivudine-resistant mutational patterns with the antiviral effect of adefovir in patients with chronic hepatitis B.
Abstract: In addition to the YMDD mutations, the rtL180M, rtL80I, and rtV173L mutations were also present in 78%, 43%, and 11% of patients, respectively.
Abstract: The rtM204V mutation always accompanied rtL180M, and rt
Abstract: The presence of the rtL180M, rtL80I, and rtV173L did not significantly affect viral load reduction during adefovir administration.
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: 19323782
2009
Liver international
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%
[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.
[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.
Evolution of primary and compensatory lamivudine resistance mutations in chronic hepatitis B virus-infected patients during long-term lamivudine treatment, assessed by a line probe assay.
PMID: 17913933
2007
Journal of clinical microbiology
Abstract: A compensatory mutation at position rt80 (L80V/I) was detected in half of these patients.
Emergence of hepatitis B virus quasispecies with lower susceptibility to nucleos(t)ide analogues during lamivudine treatment.
PMID: 17567633
2007
The Journal of antimicrobial chemotherapy
Abstract: All but three patients had baseline rtM204I/V substitutions associated with rtL180M in 23, rtL80I/V in 14, rtV173L in 4, rtT184S in 3, rtQ215S in 2 and rtA181S in 2 cases.
The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro.
PMID: 17438047
2007
Antimicrobial agents and chemotherapy
Abstract: Analysis of a large sequence database revealed that rtL80V/I occurred almost exclusively in association with LMV resistance, and 85% of these isolates encoded rtL80I.
Abstract: Collectively, these results suggest that coselection of rtL80V/I and rtM204I/V occurs because the former compensates for the loss of replication efficiency associated with the acquisition of LMV resistance, particularly in the case of rtM204I.
Abstract: Coselection of rtL80V/I occurred in 46% of isolates in which LMV resistance was attributable to
HBV mutation literature information.
PMID: 
2009
Antiviral research
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