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Viral Resistance to Ritonavir
Abstract 201
Loss of Suppression of Viral Replication by Ritonavir (ABT-538) is Quantitatively
Associated with the Acquisition of Genotypic Mutations at Codon 82 of the
HIV-1 Protease Gene.
Authors: S Eastman, R Kelso, E Boyer, M Urdea, J Kolberg, J Leonard, D Ho, M Markowitz.
This study was designed to assess the relationship between HIV RNA viral load and the development of genotypic resistance mutations during ritonavir therapy.
Seven patients with a mean CD4 count of 170 cells/mm3 were given ritonavir at 600 to 900 mg per day (the current recommended dose is 1,200 mg per day). Plasma HIV RNA levels, as measured by Chiron's bDNA assay, were reduced by a mean of 1.69 log after 2 weeks. With continued therapy, viral RNA levels returned to baseline in 6 of the 7 patients. Viral load rebound was accompanied by the development and quantitative increase in the resistance mutation at codon 82 of the protease gene. One of the 6 patients had acquired a subsequent mutation at codon 84 which resulted in further increase in viral load. A rise in viral load was observed in 3 patients following 42 days or less of ritonavir monotherapy, all of which had accompanying pre-treatment mutations at codon 63.
The study concluded that mutation at codon 82 of the HIV protease gene is associated with changes in viral load during ritonavir monotherapy. Furthermore, mutation at codon 63 may facilitate the expansion of mutant viruses with changes at codon 82 (see also Appendix C).
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