| Title | [Dissection of mechanism for the adefovir dipivoxil resistance in chronic hepatitis B patients.] | | Author(s) | Zeng AZ, Lu P, Deng H, Cai SF, Yang C, Xin XJ, Guo JJ, Li QL, Deng XH, Huang AL | | Institution | Department of Infectious Disease, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. | | Source | Zhonghua Gan Zang Bing Za Zhi 2009 Oct; 17(10):730-4. | | Abstract | OBJECTIVE: To explore the mechanism for adefovir dipivoxil (ADV) resistance occurred in chronic hepatitis B patients of a series of phase III clinical trails.
METHODS: 30 resistant HBV strains were selected out from 177 cases of ADV treated chronic hepatitis B patients. HBV polymerase RT region were amplified by nested PCR and analyzed with the standard neucleiotide sequence of HBV strains deposited in GeneBank.
RESULTS: 21 out of 30 HBV strains were primary resistant strains, among them 5 HBV strains (23.8%, 5/21) had the polymorphism site of rtN118H. While the other 9 HBV strains showed secondary resistance, variations in conservative region C (rtM207V) and other non-conservative regions were found. The classic mutation sites such as rtN236T and rtA181V/T were not found.
CONCLUSIONS: Polymorphism site of rtN118H might be responsible for HBV primary resistance to ADV therapy. rtM207V variation in HBV RT C domain and other variation sites might play a role in HBV secondary resistance to ADV treatment, and natural resistant quasispecies may be the basis for the ADV quick resistance. These conclusions await further confirmation by phenotype test. DOI: 10.3760/cma.j.issn.1007-3418.2009.10.004. | | Language | chi | | Pub Type(s) | English Abstract
Journal Article
| | PubMed ID | 19874686 |
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