Baseline HIV type 1 genotypic resistance to a newly added nucleoside analog is predictive of virologic failure of the new therapy

We evaluated the predictive value of baseline HTV-1 genotypic resistance mu tations for failure of a nucleoside reverse transcriptase inhibitor (NRTI) containing therapy. The change in therapy of 88 HIV-1-infected patients was analyzed retrospectively, relating the genotypic resistance profile at bas eline to the evolution of viral load and CD4+ T cell counts. Genotypic resi stance at baseline and at 6 months was evaluated with the LiPA HIV-1 RT, wh ich detects mutations at codons 41, 69, 70, 74, 184, and 215, At 1 to 3 mon ths after change in therapy, patients without preexisting resistance mutati ons to the new drug (group S) had a significantly better evolution in viral load (reduction of 0.37 log(10)) compared with patients with known preexis ting resistance mutation(s) (group R) (increase of 0.08 log(10)), This diff erence was particularly striking for patients with the baseline M184V mutat ion and whose treatment was modified by the addition of lamivudine. After 6 months the median difference in viral load evolution between the two group s increased to 0.61 log(10): the viral load of patients of group S was stil l 0.18 log(10) below baseline while patients of group R had an increase of 0.43 log(10) in viral load above baseline. Changes in CD4+ T cell counts we re not significantly different. The evolution in viral load in HIV-1-infect ed patients with and without baseline resistance mutation(s) toward a newly added NRTI is significantly different at 1-3 months and at 6 months after changing or adding one NRTI.