2012•Linchuang gandanbing zazhiRequires access

Evaluation of adefovir primary resistance and adefovir repulsive mutations of the HBV DNA P gene in chronic hepatitis B patients

Chunyang Li

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Abstract

Objective To determine if adefovir resistance associated with the HBV DNA P gene in chronic hepatitis B patients(CHB) results from primary or adefovir-induced mutations. Methods Seventy-eight chronic HBV patients were enrolled in the study,including 30 patients who accepted adefovir treatment and 48 patients who refused any type of nucleoside analog(NA) treatment.Serum samples from all participants were genotyped for the HBV DNA P gene by PCR amplification and automated sequencing. Results In the group of untreated patients,the main mutations were rtA181V/T10(20.8%),rtN/H238T/D/S10(20.8%),and rtV214A 13(27.1%).In the group of adefovir-treated patients,the main mutation was rtA181V/T16(53.3%),no rtN/H238T/D/S mutant was detected,and only one patient carried the rtV214A mutant of the HBV RT region. Conclusion CHB patients carry adefovir-resistance mutations that arise spontaneously,as detected in untreated patients.These resistance mutations mainly included rtV214A and rtN/H238T/D/S.However,CHB patients treated with adefovir carried less resistance mutations overall but had a much higher incidence of the rtA181V/T mutation,suggesting that this mutation may be primary or induced by adefovir.

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Objective To determine if adefovir resistance associated with the HBV DNA P gene in chronic hepatitis B patients(CHB) results from primary or adefovir-induced mutations. Methods Seventy-eight chronic HBV patients were enrolled in the study,including 30 patients who accepted adefovir treatment and 48 patients who refused any type of nucleoside analog(NA) treatment.Serum samples from all participants were genotyped for the HBV DNA P gene by PCR amplification and automated sequencing. Results In the group of untreated patients,the main mutations were rtA181V/T10(20.8%),rtN/H238T/D/S10(20.8%),and rtV214A 13(27.1%).In the group of adefovir-treated patients,the main mutation was rtA181V/T16(53.3%),no rtN/H238T/D/S mutant was detected,and only one patient carried the rtV214A mutant of the HBV RT region. Conclusion CHB patients carry adefovir-resistance mutations that arise spontaneously,as detected in untreated patients.These resistance mutations mainly included rtV214A and rtN/H238T/D/S.However,CHB patients treated with adefovir carried less resistance mutations overall but had a much higher incidence of the rtA181V/T mutation,suggesting that this mutation may be primary or induced by adefovir.

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Available abstract

Objective To determine if adefovir resistance associated with the HBV DNA P gene in chronic hepatitis B patients(CHB) results from primary or adefovir-induced mutations. Methods Seventy-eight chronic HBV patients were enrolled in the study,including 30 patients who accepted adefovir treatment and 48 patients who refused any type of nucleoside analog(NA) treatment.Serum samples from all participants were genotyped for the HBV DNA P gene by PCR amplification and automated sequencing. Results In the group of untreated patients,the main mutations were rtA181V/T10(20.8%),rtN/H238T/D/S10(20.8%),and rtV214A 13(27.1%).In the group of adefovir-treated patients,the main mutation was rtA181V/T16(53.3%),no rtN/H238T/D/S mutant was detected,and only one patient carried the rtV214A mutant of the HBV RT region. Conclusion CHB patients carry adefovir-resistance mutations that arise spontaneously,as detected in untreated patients.These resistance mutations mainly included rtV214A and rtN/H238T/D/S.However,CHB patients treated with adefovir carried less resistance mutations overall but had a much higher incidence of the rtA181V/T mutation,suggesting that this mutation may be primary or induced by adefovir.

Key concepts: Adefovir, Medicine, Chronic hepatitis, Mutation, Hepatitis B virus, Virology, Mutant, Hepatitis B

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Evaluation of adefovir primary resistance and adefovir repulsive mutations of the HBV DNA P gene in chronic hepatitis B patients — Research Paper | ScholarLens