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To the editor—The article by Margeridon-Thermet et al [1] in the May issue of the Journal shows how new technologies, such as ultra-deep pyrosequencing (UDPS), might become useful advanced diagnostic tools for the management of hepatitis B virus (HBV) infection, as they are in the management of human immunodeficiency virus (HIV) infection. Although HBV variability is limited by the presence of a double reading frame along most of the genome sequence and by the long life span of the infected cells, the virus occurs in quasispecies with a significant number of low-abundance variants [1–5], including those bearing drug resistance mutations. The role of these pre-existing variants is still controversial, because their effective selection as drug-resistant virus strains has not been demonstrated. In the case of HIV infection, the presence of low-abundance variants has been associated with a greater risk of viral treatment failure, at least for “low genetic barrier” compounds, such as nonnucleoside reverse-transcriptase inhibitors [6–8], whereas no such association has been reported for HBV. UDPS technology, with its ability to detect variants down to 1% of the quasispecies (and potentially less), could be useful in treatment-naive patients at their first treatment, but, given the slow emergence of resistance to the latest powerful drugs—entecavir and tenofovir—the most interesting results might come from studies involving patients who experience treatment failure with lamivudine and/or adefovir and are in need of a treatment change. In these patients, the presence of key minority cross-resistance mutations might alter the outcome of subsequent treatments

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