Descritta, in un “case report”, l’emersione della mutazione N88S. E’ su un paziente pre-trattato, che era resistente a SQV,che ha utilizzato ATV/rtv dopo che aveva acquisito 118 cp/ml di carica virale. Particolare l’analisi dell’evoluzione virale.

E’ il primo caso, a conoscenza degli autori, dell’emersione di una mutazione differente dalla classica I50L, quella segnalata con l’utilizzo di solo atazanavir. Riportiamo integralmente la descrizione del caso:

Briefly, the patient who is the subject of the report had prior antiretroviral experience with SQV and immediately prior to beginning a regimen that included ATV had a viral load (VL) of 6,547 copies/mL and a CD4 count of 445 cells/mm3 on non-PI HAART.

Resistance testing at that time revealed no phenotypic or genotypic PI resistance. The patient was begun on an ATV, tenofovir/TDF (Viread), abacavir/ABC (Ziagen)and lamivudine/3TC (Epivir) regimen, and at 3 months the patient’s VL had fallen to 118 copies/mL.

Thereafter, RTV was added to dose adjusted ATV and while the subsequent VL was <50 copies/mL, it gradually rose to 7,535 copies/mL 7 months later.

The protease genotype at that time revealed K20T, M36I/V, L63P, A71T, and N88S.

The HIV phenotype showed susceptibility (fold change) to ATV, APV, IDV, LPV, NFV, and SQV was 56, 0.3, 13, 4.3, 68, and 4.2, respectively, and that replication capacity, which was 96% prior to ATV, was 14%.

Reference:
E Coakley and others. Atazanavir Resistance in a Protease Inhibitor (PI) Naïve Patient Treated with Atazanavir/Ritonavir Associated with Development of the N88S Mutation in Protease. 12th Conference on Retroviruses and Opportunistic Infections. Boston, MA; February 22-25, 2005. Abstract 716.