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Many studies have demonstrated that the long-term, virological, immunological and clinical effectiveness of highly active antiretroviral therapy (HAART) is mainly related to durable suppression of viral replication. Among the specific antiretroviral agents available today, nelfinavir has been widely used in the last 3 years. This open label, non comparative, retrospective study on 307 patients living with HIV aimed to evaluate the effectiveness of an antiretroviral (ART) regimen including nelfinavir as first-line HAART in terms of rate and durability of viro-immunological response. Most patients, 258/307 (84%), were pre-treated whereas only 49/307 (16%) were treatment naive. The median baseline CD4 cell count was 223 cells/mm(3) for naive patients and 317 cells/mm(3) for experienced patients whereas median HIV RNA values were 2,500 and 82,000 copies/ml for experienced and naive patients respectively. Median times spent on nelfinavir were 839 and 897 days for experienced and naive patients respectively, with 171/258 pre-treated patients (66%) remaining on nelfinavir-based therapy up to 24 months. Overall, the mean CD4 increase was 196 cells/mm(3) with a relevant increment of 165 in experienced patients and 367 cells/mm3 in naive patients (p

The best salvage therapy for protease inhibitor (PI)-resistant HIV-infected patients is still controversial. We measured changes in viral load and CD4 T-lymphocyte counts in 40 PI-resistant patients receiving boosted PI-including or PI-sparing antiretroviral therapy. At multivariate analysis, the only independent predictor of CD4 T-lymphocyte changes at week 24 was a boosted PI-including regimen. In PI-resistant HIV-infected patients, a boosted PI regimen preserves CD4 T lymphocytes from depletion in the medium term compared with a PI-sparing regimen.

To understand the evolutionary characteristics of HIV- 1 variants resistant to protease inhibitors ( PI), the replicating plasma virus was analyzed in three patients shifted to a PI- sparing regimen after virological failure. The dynamic features of carryover of mutations associated with PI resistance in the absence of selective pressure on the protease gene indicate that viral variants resistant to reverse transcriptase inhibitors and bearing mutations of the protease sequence can maintain efficient replication capacity in vivo.