Introduction: In addition, studies have observed that amino acid (AA) substitutions in other positions of RT, such as rtV191I and rtT128I/N, were selected during prolonged NA therapy and affected the replication capacity of HBV.
Ultra-deep pyrosequencing detects conserved genomic sites and quantifies linkage of drug-resistant amino acid changes in the hepatitis B virus genome.
Result: At the time of LMV VBK (sample 4C), percentages of rtA181T (71.7%), rtM204V (5.6%), and rtL180M (5%) notably increased relative to baseline samples, as did other LMV resistance substitutions, particularly rtV191I (5.8%), rtV207I (3.9%), and rtV173L (1.4%), although to a lesser extent.
Discussion: In this sense, the increase in percentages of NA-resistant rtV191I in the absence of treatment concurs with its reported link to humoral immune response escape by an association with the
Characterization of drug-resistance mutations in HBV D-genotype chronically infected patients, naive to antiviral drugs.
Abstract: Additionally, five polymorphic mutations, with a suggested role in drug resistance, were detected [rtQ215S (12.8%), rtI233V (4.3%), rtV214A (3.6%), rtV191I (0.7%), rtV207L (0.7%)].
Abstract: Amino acid changes at other six RT positions, potentially associated with resistance, were also analyzed (rtV84M-rtV191I-rtV207L-rtV2
Molecular analysis of an HBsAg-negative hepatitis B virus mutant selected in a tenofovir-treated HIV-hepatitis B virus co-infected patient.
Abstract: The molecular analysis performed in an HIV-hepatitis B virus (HBV) coinfected patient revealed selection of an unusual HBV polymerase mutation (rtV191I) during tenofovir-containing therapy, conferring simultaneously immune escape by HBsAg negativity and resistance to lamivudine but not tenofovir.
Evolution of hepatitis B virus polymerase mutations in a patient with HBeAg-positive chronic hepatitis B virus treated with sequential monotherapy and add-on nucleoside/nucleotide analogues.
Abstract: At week 22 during ADV treatment, LAM-resistance mutations (rtL180M, rtT184L, rtM204I, rtV191I, and rtL229V) were not detected.
Abstract: Two new mutations, rtL229V and rtV191I, were detected in 75.0% (33/44) and 11.4% (5/44) of clones, respectively.
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
Result: Three of the 13 residues with stop codons were always associated with RT amino acid mutations, of which 2 (rtA181T and rtV191I) have previously been reported.
HBV mutation literature information.
PMID: 
2013
Virology journal
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