COMMENTARY

Lamivudine therapy

Resistance to lamivudine therapy: is there more than meets the eye?

G Dusheiko, A Bertoletti

Centre for Hepatology and Institute for Hepatology, Royal Free and University College School of Medicine, London, UK

Correspondence to:
Correspondence to:
Professor G Dusheiko
Centre for Hepatology and Institute for Hepatology, Royal Free and University College School of Medicine, Pond St, London HA5 1DE, UK; g.dusheiko@rfc.ucl.ac.uk

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A CD8+ T cell response to lamivudine resistant polymerase cytotoxic T lymphocyte (CTL) epitope influences the response to lamivudine treatment for chronic hepatitis B and may indicate an important aspect of the role of T cell responsiveness in lamivudine therapy

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Keywords: chronic hepatitis B; cytotoxic T lymphocyte activity; lamivudine therapy; tetramer assay; YMDD motif

The first 150 words of the full text of this article appear below.

The goals of treatment of hepatitis B are to prevent progression of the disease or to slow the disease process. Hepatitis B virus (HBV) is a DNA virus which integrates into the host genome. Thus it is difficult to eradicate viraemia. However, it is possible, albeit in a minority, to reduce levels of viraemia to relatively low threshold levels after finite courses of treatment with either interferon alpha or nucleoside analogues, and to lessen the induced necroinflammatory and immune response.¹ Two major forms of active chronic hepatitis B are recognised: wild-type (or hepatitis B e antigen (HBeAg) positive chronic HBV infection) and anti-HBe positive or precore mutant disease. The latter disease is caused by variants of HBV that contain nucleotide substitutions in the core promoter/precore regions of the viral genome.²

Wild-type (HBeAg positive) chronic hepatitis B can be treated with either interferon alpha or nucleoside analogues. Loss of . . . [Full text of this article]

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