Selection and counterselection of the rtI233V adefovir resistance mutation during antiviral therapy.
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Selection and counterselection of the rtI233V adefovir resistance mutation during antiviral therapy. / Schildgen, Oliver; Olotu, Cynthia; Funk, Anneke; Zöllner, B.; Helm, Martin; Rockstroh, Jürgen Kurt; Sirma, Hüseyin.
In: J CLIN MICROBIOL, Vol. 48, No. 2, 2, 2010, p. 631-634.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Selection and counterselection of the rtI233V adefovir resistance mutation during antiviral therapy.
AU - Schildgen, Oliver
AU - Olotu, Cynthia
AU - Funk, Anneke
AU - Zöllner, B.
AU - Helm, Martin
AU - Rockstroh, Jürgen Kurt
AU - Sirma, Hüseyin
PY - 2010
Y1 - 2010
N2 - 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.
AB - 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.
M3 - SCORING: Journal article
VL - 48
SP - 631
EP - 634
JO - J CLIN MICROBIOL
JF - J CLIN MICROBIOL
SN - 0095-1137
IS - 2
M1 - 2
ER -