Background: The main objective was to evaluate in Acute HIV Seroconverters (AHS) the ability of a 34-week (wk) continuous HAART followed by a 50-wk period of HAART with Structured Treatment Interruptions (STIs) to induce anti-HIV immune response and control HIV replication after HAART cessation.

Methods: Patients (pts) presented with symptoms of primary infection and at least 2 of the following criteria within 4 wks prior to inclusion: 1) positive p24 antigenemia; 2) negative or weakly positive HIV ELISA; 3) £ 3 bands on HIV Western blot. HAART combined didanosine, stavudine, nelfinavir, and hydroxyurea, given continuously for 34 wks. Afterwards, pts with plasma viral load (PVL) < 20 copies (c)/ml entered the STI phase that consisted of 3 periods of 2, 4, and 8 wks off HAART, each separated by 12 wks on HAART. HAART was permanently stopped at wk 84 and pts were followed up until wk 108. Criteria for resuming HAART were either occurrence of symptoms consistent with acute infection, PVL > 50,000 c/ml, or CD4 < 300/mm³. CD4 anti-HIV activity was assessed by both proliferation assay and g-IFN synthesis (ELISPOT assay) using the gag p24 antigen.

Results: Twenty-nine (29) AHS (23 M/6 F, mean age 34 years) were enrolled. Median baseline PVL and CD4 were 5.25 log₁₀/ml and 476/mm³, respectively. As of October 2002, 2 pts were lost to follow-up; 27 pts had completed the 3 STIs; 14 had reached wk 84 and stopped HAART; and 8 had reached wk108. HU had been withdrawn in 15 pts for peripheral neuropathy (n = 5), oral ulcerations (n = 3), laboratory abnormalities (n = 3), or other reasons (n = 4). Viral rebound was observed in all pts during all 3 STIs, which occurred without clinical symptoms, significant CD4 count drop or deleterious effect on anti-HIV CD4 responses. Median PVL tended to decrease from 1^st to 3^rd STI when measured 2 wks after each STI (3.8, 3.2, and 2.8 log₁₀/ml, respectively), but not when considering peak PVL within each STI (3.8, 3.8, and 4.0 log₁₀/ml, respectively). None of the 8 pts who reached wk 108 had persistent PVL < 20 c/mL. However, HAART had been resumed in none of them, and 2 pts had PVL persistently < 400 c/ml. The percentage of pts who exhibited significant anti-HIV CD4 responses increased 3- to 4-fold from baseline to wk 108.

Conclusions: Although viral rebound at wk 2 post-STI tended to decrease from 1^st to 3^rd STI, maximum viral rebound within each STI did not. So far, persistent control of HIV replication after cessation of a 2-year HAART/STI regimen was observed in a small minority of pts.