Selection and Counterselection of the rtI233V Adefovir Resistance Mutation during Antiviral Therapy

Recently, we reported on three patients with chronic hepatitis B virus (HBV) infection for whom adefovir (ADF) therapy virologically failed, most likely due to a preexisting rtI233V HBV polymerase mutation. Here, we describe two further patients with chronic HBV infection who were found to develop t...

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Bibliographic Details
Published in:Journal of Clinical Microbiology 2010-02, Vol.48 (2), p.631-634
Main Authors: Schildgen, Oliver, Olotu, Cynthia, Funk, Anneke, Zöllner, Bernhard, Helm, Martin, Rockstroh, Jürgen Kurt, Sirma, Hüseyin
Format: Article
Language:English
Subjects:
Adenine - analogs & derivatives
Adenine - pharmacology
Adenine - therapeutic use
Adult
Amino Acid Sequence
Amino Acid Substitution - genetics
Antiviral Agents - pharmacology
Antiviral Agents - therapeutic use
Biological and medical sciences
Drug Resistance, Viral
Female
Fundamental and applied biological sciences. Psychology
Guanine - analogs & derivatives
Hepatitis B virus
Hepatitis B virus - drug effects
Hepatitis B virus - genetics
Hepatitis B virus - isolation & purification
Hepatitis B, Chronic - drug therapy
Hepatitis B, Chronic - virology
Humans
Male
Microbiology
Molecular Sequence Data
Mutation, Missense
Organophosphonates - pharmacology
Organophosphonates - therapeutic use
Selection, Genetic
Sequence Alignment
Tenofovir
Treatment Failure
Viremia
Virology
Young Adult
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Summary:Recently, we reported on three patients with chronic hepatitis B virus (HBV) infection for whom adefovir (ADF) therapy virologically failed, most likely due to a preexisting rtI233V HBV polymerase mutation. Here, we describe two further patients with chronic HBV infection who were found to develop the rtI233V mutation after initiation of ADF therapy. These patients represent the first cases known so far in which the rtI233V ADF resistance mutation evolved under persistent HBV replication during HBV therapy with ADF. Interestingly, one of the previously described patients, who was initially successfully switched from ADF to tenofovir (TDF) and became virologically suppressed subsequently, experienced a moderate but remarkable rebound of HBV viremia after switching from TDF to entecavir, due to the emergence of renal toxicity. Thus, we provide evidence for the selection and counterselection of the rtI233V ADF resistance mutation during antiviral therapy.
ISSN:0095-1137
1098-660X
DOI:10.1128/JCM.01073-09