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Determinants of Virologic and Immunologic Outcomes in Chronically HIV-Infected Subjects Undergoing Repeated Treatment Interruptions

2007; Lippincott Williams & Wilkins; Volume: 46; Issue: 1 Linguagem: Inglês

10.1097/qai.0b013e31813e62e1

1944-7884

Lucia Palmisano, Marina Giuliano, Raffaella Bucciardini, Vincenzo Fragola, Mauro Andreotti, Clementina Maria Galluzzo, Maria Franca Pirillo, Liliana Elena Weimer, Romano Arcieri, Elena Germinario, Roberta Amici, Maria Grazia Mancini, Antonella d’Arminio Monforte, Francesco Castelli, P Caramello, Stefano Vella,

HIV Research and Treatment

Factors influencing the outcome of structured treatment interruptions (STIs) in HIV chronic infection are not fully elucidated.In ISS-PART, 273 subjects were randomly assigned to arm A (137 assigned to continuous highly active antiretroviral therapy [HAART]) and arm B (136 assigned to 5 STIs of 1, 1, 2, 2, and 3 months' duration, each followed by 3 months of therapy). Main outcome measures were the proportion of subjects with a CD4 count >500 cells/mm3, the rate of virologic failure, and the emergence of resistance at 24 months.The proportion of subjects with a CD4 count >500 cells/mm3 was higher in arm A than in arm B (86.5% vs. 69.1%; P = 0.0075). Pre-HAART CD4 cell count and male gender were independent predictors of a CD4 count >500 cells/mm3 in arm B. The overall risk of virologic failure was not increased in arm B; however, it was higher in the 38 subjects who had resistance mutations in the rebounding virus. Archived mutations at baseline and the use of a regimen that included an unboosted protease inhibitor (PI), compared with nonnucleoside reverse transcriptase inhibitor-based HAART, independently predicted the emergence of plasma mutations during STI (P = 0.002 for DNA mutations and P = 0.048 for PI-based HAART).Our results suggest that patients with preexisting mutations and treated with unboosted PI-based HAART should not be enrolled in studies of time-fixed treatment interruptions, being at higher risk of developing plasma mutations during STI and virologic failure at therapy reinstitution.