Result: The MRT revealed I169L mutation in one patient (Fig 4, Table 4).
Table: I169L
Discussion: A single HBV strain has an I169L mutation, at a position associated with resistance to Entecavir, although leucine (L) is not the amino acid involved.
Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia.
Abstract: The L180M and M204V resistance mutations were simultaneously identified in one sample, while the I169L resistance mutation was identified in another one.
Discovery of the Novel Entecavir-Resistant Hepatitis B Virus Reverse Transcriptase A181C Substitution From an Integrated Genotypic Analysis.
Result: We also screened several mutations relevant to antiviral resistance, such as I169L, L180M, A181V, T184I, S202C, M204V/I, N236T and M250I in the RT region.
HBV Drug Resistance Substitutions Existed before the Clinical Approval of Nucleos(t)ide Analogues: A Bioinformatic Analysis by GenBank Data Mining.
Result: However, the relationship between other atypical AA substitutions with susceptibility to NUCs has not been characterized in vitro, such as rtI169L (not typical rtI169T) and rtM204L (not typical rtM204I/V).
Discussion: In addition, we found that the detected atypical substitutions of rtI169L, rtA181G, rtS202T/R, rtM204L, and rtM250K were not
Antiviral efficacy of adefovir dipivoxil in the treatment of chronic hepatitis B subjects from Indian subcontinent.
PMID: 24399391
2014
Indian journal of medical microbiology
Abstract: On sequence analysis, two subjects were identified with rtI169L and rtA181V mutation after 9 months and 18 months of adefovir treatment, respectively.
A deep-sequencing method detects drug-resistant mutations in the hepatitis B virus in Indonesians.
8Discussion: The mutation at sF161H, which is located adjacent to the region that was defined as the ""a"" determinant, in association with rtI169L mutation was observed in patient 1, 3, and 4."
Abstract: Patient 4 had mutations at T128N (1%), I169L (1%), V173L (2%), A181V (1%), and Q215H (1%).
Discussion:
Discussion: Unlike the previous study, rtI169S/L and/or rtS202G mutations were detected in the absence of LAM resistance variants at pretreatment, even though those variants disappeared during LAM therapy until VB.
Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome.