The replication capacity and drug sensitivity of Adefovir dipivoxil-resistant HBV mutants in vivo.
- Author:
Jun LEI
1
;
Zhan GAO
;
Lu XU
;
Li LIU
;
Hong TANG
Author Information
1. The Center of Infectious Diseases, West China Hospital of Sichuan University, Division of Infectious Diseases, State Key Laboratory of Biotherapy, Sichuan University, Chengdu 610041, China.
- Publication Type:Journal Article
- MeSH:
Adenine;
analogs & derivatives;
pharmacology;
Animals;
Antiviral Agents;
pharmacology;
Base Sequence;
Drug Resistance, Viral;
genetics;
Hepatitis B;
drug therapy;
virology;
Hepatitis B virus;
drug effects;
genetics;
Male;
Mice;
Mice, Inbred BALB C;
Molecular Sequence Data;
Mutagenesis, Site-Directed;
Mutation;
Organophosphonates;
pharmacology
- From:
Journal of Biomedical Engineering
2011;28(1):125-128
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to research the changes of the biological characteristics of Hepatitis B virus-resistant mutant model in vivo. The anti-ADV mutant HBV plasmid of rtA181V and rtN236T, prepared by Multi Site-Directed Mutagenesis Kit, was transferred into mice via the tail vein, and the levels of HBV-DNA replication were detected after Anti-HBV drugs treatment. The HBV-DNA replication had been detected in the mutant mice, which means that the establishment of HBV-resistance mutant model in vivo was successful, but the level of HBV DNA replication intermediates in the anti-ADV mutant mice liver were decreased compared with wild 4.1kb HBV plasmid mice. The wild-type mice were sensitive to Lamivudine, Adefovir dipivoxil and Entecavir. Though the mutant mice were also sensitive to Entecavir, the sensitivity to lamivudine and Adefovir dipivoxil decreased. As a result, this study established the Adefovir-resistant hepatitis B virus mouse model successfully. However, the replication level of HBV-DNA was reduced in this model, and Adefovir dipivoxil in the mutant mice had no significant inhibition effect on HBV-DNA.
