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Reyataz Viral Response in Experienced Patients -genotypic mutation score
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"Virological response following switch to atazanavir/ritonavir in relation to baseline genotypic resistance pattern"
ABSTRACT 149
Antiviral Therapy 2004; 9:S165.
S Yerly, S Vora, H Günthard, P Vernazza, H Furrer, A Zinkernagel, B Hirschel, L Perrin and the Swiss HIV Cohort Study (SHCS)Laboratory of Virology, Genève Hospital, Switzerland
BACKGROUND: Genotypic correlates of HIV-1 resistance to atazanavir (ATV) have been described. Our aim was to assess virological response and to identifyclinically relevant genotypic scores for resistance to ATV/ritonavir (RTV) in treatment experienced patients.
METHODS: PI-experienced patients from the SHCS who were switched to ATV/RTV (2•150 mg ATV, 100 mg RTV, QD) containing HAART with HIV-1 RNA >1000 copies/ml at baseline were included. The impact of baseline protease mutations on virological response at 3 months was analysed.
RESULTS: Data of the first 25 patients (3 months follow- up) were included in this analysis. Median baseline viraemia and CD4 count were 4.88 log10 copies/ml and 133/mm3, respectively. Patients had been treated with a median of three PIs (range 1--6).
Reason for switch was virological failure (n=18), poor adherence (n=4) and drug intolerance (n=3). The median number of active drugs associated with ATV/RTV was 2 (0--4).
At 3 months, the median viraemia decrease was --2.09 log10 copies/ml (--4.72 to 0.39) with 19 (76%) patients presenting HIV-1 RNA <400 copies/ml and/or >1 logdecrease. The median baseline number of mutations associated with PI-resistance [IAS] was 5 (range, 0 to 14) and the median number of mutations associated with ATV resistance [according to R Colonno: 10, 20, 24, 33, 36, 46, 48, 54, 63, 71, 73, 82, 84, and 90] was 3 (0 to 9).
This ATV resistance score predicted 12/25 patients as resistant, but 6 (50%) of them were responders. In non-parametric univariate analyses, the proteasemutations associated with a reduced virological response to ATV/RTV were 10, 20, 32, 33, 46, 47, 54, 82, 84, and 90 (P<0.05).
There was a correlation between the number of PI mutations and virologicalresponse at 3 months (r=0.66, P<0.0001). A genotypic score derived from extended data will be presented.
CONCLUSION: Despite mutations associated with ATV-resistance, we have observed significant virological response in protease inhibitor and nucleoside reverse transcriptase-experienced patients who were switched to a genotype guided optimised salvage regimen containing boosted ATV.
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