Complex genotypic changes during failure of HBV nucleoside analogue therapy

Deenan Pillay*, David Mutimer, Nigel Burroughs, David Cooper, Patricia Cane

*Corresponding author for this work

    Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

    Abstract

    This chapter focuses on clinical studies of hepatitis B virus (HBV) antiviral drugs and the HBV genotype. Infection in three groups of treated patients are considered-namely, (1) liver transplant recipients given HBV to prevent re-infection, (2) chronic HBV infected patients, and (3) HBV/human immunodeficiency virus-1 (HIV-1)-coinfected patients. The chapter explores the emergence of HBV drug resistance against lamivudine in a range of patient groups. A range of nucleoside analogues have activity against hepatitis B virus (HBV), including lamivudine, famciclovir, and entecavir. Differences in the dynamics of emergence of resistance between transplant and non-transplant patients have been identified through detailed virological monitoring and genotypic analysis of HBV polymerase. The monotherapy drug pressure selects for a wide range of viral species, the presence of which compromise subsequent nucleoside analogue therapy. It is essential that the new strategies for therapy of HBV are based on highly potent combination regimens, thereby reducing the risk of emergence of drug resistance.

    Original languageEnglish
    Title of host publicationFrontiers in Viral Hepatitis
    PublisherElsevier Inc.
    Pages353-364
    Number of pages12
    ISBN (Print)9780444509864
    DOIs
    Publication statusPublished - Dec 2003

    Fingerprint

    Dive into the research topics of 'Complex genotypic changes during failure of HBV nucleoside analogue therapy'. Together they form a unique fingerprint.

    Cite this