Baseline CD4 count was normal in both patients, except that patient B had a below-normal percentage relative to total lymphocytes. From day 360, both patients remained within normal ranges (table). Plasma RNA was positive at baseline (patient A: 676 copies/mL; patient B: 1120 copies/mL), became undetectable by day 360 and remained undetectable after 12 months’ suspension of treatment, in both patients. Baseline proviral DNA in the PBMC was quantified at 654 copies/106 cells in patient A and 65 copies/106 cells in patient B. At days 360 and 720, proviral DNA was non-quantifiable in patient B, and marginally detectable in patient A. Qualitative evaluation of proviral DNA in PBMC in triplicate experiments at day 720 showed low amplification of the pol region in both patients (one of three samples positive), and of the gag region (one of three samples positive for patient A, and two of three positive for patient B). To assess whether proviral DNA detected was competent for transcription, we tested for intracellular HIV-RNA. Baseline intracellular RNA in the PBMC was quantifiable in both patients but was undetectable at day 360 and remained undetectable despite the absence of treatment. We were unable to isolate any infectious virus from the PBMC.

At day 360, lymphnode viral load was undetectable in patient A; in patient B, 26 copies of proviral DNA per 106 cells was found. One year after treatment was stopped, very low levels of proviral DNA were found in lymphnodes of both patients. The presence of provirus was confirmed by qualitative analysis (amplification of gag positive for both patients, and amplification of pol positive for patient B and negative for patient A). However, no extracellular nor intracellular HIV RNA was detectable at day 720 in either