alexa Mutation Patterns at Codons Rt204 And Rt180 of the HBV Polymerase Gene Associated with Lamivudine Resistance in Treated and Untreated Chronic HBV Patients in Kuwait: A Case Series | Abstract
ISSN: 2165-7920

Journal of Clinical Case Reports
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Case Report

Mutation Patterns at Codons Rt204 And Rt180 of the HBV Polymerase Gene Associated with Lamivudine Resistance in Treated and Untreated Chronic HBV Patients in Kuwait: A Case Series

Maisa Mahmoud Ali1*, Fuad Hasan1,2, Suhail Ahmad1, Siham Al-Mufti3, Haifa Asker4, Salem Farhan5 and Widad Al-Nakib5
1Department of Microbiology, Faculty of Medicine, Health Sciences Center, Kuwait University, Kuwait
2Department of Medicine, Faculty of Medicine, Health Sciences Center, Kuwait University, Kuwait
3Public Health Laboratories, Shaab, Ministry of Health, Kuwait.
4Gastroenterology Unit, Al-Amiri Hospital, Ministry of Health, Kuwait
5Department of Microbiology, Faculty of Medicine, Health Sciences Center, Kuwait University, Kuwait
Corresponding Author : Maisa Mahmoud Ali
Faculty of Medicine, Department of Microbiology
Health Sciences Center, Kuwait University
PO Box 24923, Safat 13110, Kuwait
Tel: +965-2498-6503
Fax: +965-2531-8454
E-mail: [email protected], [email protected]
Received March 27, 2013; Accepted May 10, 2013; Published May 13, 2013
Citation: Ali MM, Hasan F, Ahmad S, Al-Mufti S, Asker H, et al. (2013) Mutation Patterns at Codons Rt204 And Rt180 of the HBV Polymerase Gene Associated with Lamivudine Resistance in Treated and Untreated Chronic HBV Patients in Kuwait: A Case Series. J Clin Case Rep 3:276. doi:10.4172/2165-7920.1000276
Copyright: © 2013 Ali MM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Introduction: Lamivudine is a potent inhibitor of hepatitis B virus (HBV) replication via suppression of the RNAdependent DNA polymerase. However, patients with prolonged therapy were previously detected harboring drugresistant mutants. Such mutants though partially replication defective, confer resistance to lamivudine and can elicit exacerbation of hepatonecro-inflammation. Cases presentation: In this case series, we examined mutations in the YMDD motif gene in five lamivudinetreated patients (60 yr male, 50 yr female, 46 yr male, 36 yr male and 42 yr male) and in four untreated patients (34 yr female, 29 yr male, 29 female and 37 yr male). Rare mutational patterns of rtM204L in conjunction with rtL108M were recognized conferring resistance to lamivudine. The rtL180M compensatory mutation was identified in conjunction with rtM204V/I/L; among which three patients had viral and biochemical breakthrough associated with serum HBV DNA levels exceeding 106 copies/mL. Conclusions: These results indicate that; (i) lamivudine resistant HBV strains are naturally occurring mutants as detected in lamivudine untreated patients and; (ii) New mutational patterns (rtM204L: YLDD and rtL180M) were identified conferring resistance to lamivudine and resulted in biochemical and virological breakthrough. Based on these findings, we propose that such mutations can be used as a marker to predict development of viral breakthrough in the HBV patients whether or not treated with lamivudine.

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