Selection of a hepatitis B virus strain resistant to adefovir in a liver transplantation patient

Villeneuve, Jean‐Pierre; Durantel, David; Durantel, Sandra; Westland, Christopher; Xiong, Shelly; Brosgart, Carol; Gibbs, Craig S.; Parvaz, Parviz; Werle, Bettina; Trépo, C.; Zoulim, Fabien

doi:10.1016/j.jhep.2003.09.022

Cited by 281 publications

(251 citation statements)

References 30 publications

(25 reference statements)

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“…Previous in vitro studies have shown that ADV-resistant HBV strains were susceptible to ETV. [17][18][19] Although increasing evidence supports the therapeutic efficacy of ETV in LAMr patients, [13][14][15] limited clinical data are available on ADV-resistant patients showing prior LAM resistance. 20,21 A small cohort study showed that switching to ETV plus ADV was highly efficient in 13 CHB patients who failed sequential or combination therapy with LAM and ADV, with a 76.9% (10/13) HBV DNA clearance rate during a median 10 months of treatment (range, 4-16 months).…”

Section: Discussionmentioning

confidence: 99%

Efficacy of entecavir in patients with chronic hepatitis B resistant to both lamivudine and adefovir or to lamivudine alone

et al. 2009

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Entecavir (ETV) is currently recommended as a rescue therapy purely for adefovir (ADV)-resistant chronic hepatitis B virus (HBV) infections.We evaluated the efficacy of ETV in patients who were resistant to lamivudine (LAM)/ADV sequential therapy and in those resistant to LAM monotherapy. Fifty LAM/ADV-resistant and 38 LAM-resistant patients who received ETV 1 mg/day for at least 48 weeks were enrolled. Mean baseline serum HBV DNA and alanine aminotransferase (ALT) levels were significantly lower in the LAM/ADVresistant group, compared with the LAM-resistant group (6.90 versus 7.62 log 10 copies/mL and 102.6 versus 160.2 IU/L; both P < 0.05); hepatitis B e antigen (HBeAg) status and LAM-resistant mutation patterns were similar in the two groups. At week 48, mean reductions in HBV DNA and ALT levels were significantly less in the LAM/ADV-resistant group (؊2.96 versus ؊4.86 log 10 copies/mL and ؊68.3 versus ؊128.9 IU/L; both P < 0.05). Achievement of undetectable HBV DNA was also less common in the LAM/ADV-resistant group (10.0% versus 34.2%; P ‫؍‬ 0.006), although the rates of HBeAg loss and ALT normalization did not differ between the two groups. Resistance to both LAM and ADV was an independent risk factor for failure of HBV DNA negativity at week 48 (odds ratio, 0.138; P ‫؍‬ 0.019). In both LAM/ADV-resistant and LAM-resistant groups, primary responders (>1 log decline in HBV DNA at week 12) achieved a significantly greater decrease in HBV DNA levels over the 48-week period, compared with primary nonresponders (؊4.18 versus ؊0.97 and ؊5.37 versus ؊2.15 log 10 copies/mL, respectively; both P < 0.05). Conclusion:The 48-week ETV treatment was less effective in LAM/ADV-resistant than in LAM-resistant patients. Continuing ETV monotherapy could be determined based on the virological response at 12 weeks in LAM/ADV-resistant patients. (HEPATOLOGY 2009;50:1064-1071

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Section: Discussionmentioning

confidence: 99%

Efficacy of entecavir in patients with chronic hepatitis B resistant to both lamivudine and adefovir or to lamivudine alone

et al. 2009

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“…38 This function can provide insights into the significance of a mutation in relation to antiviral drug resistance and potential mechanism for antiviral resistance. 38,39 The European Network of Excellence on antiviral drug resistance management, ViRgil, is also developing a database using a common clinical record form and a centralized virology laboratory.…”

Section: Hbv Resistance Databases and Virtual Phenotypingmentioning

confidence: 99%

Antiviral drug-resistant HBV: Standardization of nomenclature and assays and recommendations for management

et al. 2007

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“…They are frequently associated with compensatory mutations in the conserved B domain (rtV173L, rtL180M) that restore partially the replicative capacity of YMDD mutant strains in vitro 13,14 , and are associated with a 1000-fold reduction in the susceptibility to the drug 15 . Adefovir-resistance is associated with the selection of the rtN236T mutation within the D domain of the viral enzyme or with a rtA181V amino acid change in the B domain of the RT [16][17][18] . The rtN236T mutation induces a reduction in the susceptibility to adefovir by 3 to 6 fold compared to wild-type HBV (wt) in vitro, but retains some level of susceptibility to lamivudine 16,17,19 .…”

Section: Chronic Hepatitis B Virus (Hbv) Infection Remains a Major Hementioning

confidence: 99%

“…Adefovir-resistance is associated with the selection of the rtN236T mutation within the D domain of the viral enzyme or with a rtA181V amino acid change in the B domain of the RT [16][17][18] . The rtN236T mutation induces a reduction in the susceptibility to adefovir by 3 to 6 fold compared to wild-type HBV (wt) in vitro, but retains some level of susceptibility to lamivudine 16,17,19 .…”

Section: Chronic Hepatitis B Virus (Hbv) Infection Remains a Major Hementioning

confidence: 99%

Selection of a Multiple Drug-Resistant Hepatitis B Virus Strain in a Liver-Transplanted Patient

et al. 2006

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Selection of a hepatitis B virus strain resistant to adefovir in a liver transplantation patient

Cited by 281 publications

References 30 publications

Efficacy of entecavir in patients with chronic hepatitis B resistant to both lamivudine and adefovir or to lamivudine alone

Efficacy of entecavir in patients with chronic hepatitis B resistant to both lamivudine and adefovir or to lamivudine alone

Antiviral drug-resistant HBV: Standardization of nomenclature and assays and recommendations for management

Selection of a Multiple Drug-Resistant Hepatitis B Virus Strain in a Liver-Transplanted Patient

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