Background: HIV cannot be eradicated even when HAART is started early in the course of primary infection. The main objective of this trial was to evaluate the capacity of a treatment regimen consisting of a 34-week HAART induction phase followed by a 50-week STI phase to induce specific anti-HIV immune response and effective control of HIV replication in patients with symptomatic primary HIV-1 infection.

Methods: Patients presented or had presented with symptoms of primary infection and had at least 2 of the following criteria within 4 weeks prior to inclusion: positive p24 antigenemia; negative or weakly positive HIV ELISA; and no more than 3 bands on HIV Western blot test. HAART (combined didanosine, stavudine, nelfinavir, and hydroxyurea), was given continuously for 34 weeks. Patients who had undetectable (<20 copies/mL) plasma viral load (PVL) entered the STI phase that consisted of 3 periods of 2, 4, and 8 weeks off therapy, each followed by 12 weeks on therapy. HAART is to be stopped at week 84 and patients will be followed up until week 108. Criteria for resuming HAART are the following: occurrence of symptoms consistent with acute infection, PVL>50,000 copies/mL, or CD4<300/mm³. CD4 specific anti-HIV activity was assessed by ELISPOT assay that determined the frequency of cells producing IFN-g against p24 antigen. CD8 specific anti-HIV activity was assessed using similar techniques towards env, gag, pol, and nef antigenic peptides.

Results: 29 acute seroconverters (23 males, 6 females, mean age 34 years) were enrolled. Median baseline PVL and CD4 were 5.25 log₁₀/mL and 476/mm³, respectively. As of September 2001, 16 patients completed the induction phase, 13 of whom underwent first STI; 9 of 10 and 4 of 4 patients underwent the second and third STIs, respectively. HU was withdrawn in 3 patients because of peripheral neuropathy, and in 4 other patients because of other adverse events, none of which was graded severe. Only 1 patient was lost to follow-up. During first STIs, all patients experienced viral rebound without clinical symptoms, significant CD4 count decrease, or deleterious effect on anti-HIV CD4 responses. At the end of the second STI, median PVL was 0.8 log lower than after the first STI (p<0.05) and 1.7 log lower than at baseline (p<0.05) in the 9 patients assessed; and median HIV DNA were 0.7 log lower than at baseline (p<0.03) in the 7 patients assessed.

Conclusion: STIs can be performed safely in patients with acute seroconversion. Results will be updated and preliminary data on specific immune responses will be presented.