Results. Patients with HIV controller status were rare, comprising! 1% of HIV-infected patients who were followed up in an infectious diseases department and/or were participating in the French prospective SEROCO-HEMOCO cohort, but the frequency of this condition was similar in each cohort. All patients had a positive HIV serologic titer. Their characteristics are given in table 1. All patients had stage A HIV infection, according to the Centers for Disease Control and Prevention classification, and were asymptomatic. Two patients had chronic hepatitis B, and 7 had chronic hepatitis C. Results of tests for detection of antiretroviral drugs in plasma specimens from patients in group A were negative. The median CD4+ T cell count was cells/L (range, 6 750 10 280–1398 cells/L) in group A and cells/L (range, 332–6 750 10 1225 cells/L) in group B. Patients had a stable CD4+ T cell count over time: 3 had a CD4+ T cell count with a slope of 0 (mean change in the CD4+ T cell count, cells/year), 10 0 5 had a CD4+ T cell count with a slightly negative slope (mean decrease, 21 cells/year; range, 6–40 cells/year), and 2 had a CD4+ T cell count with positive slope (mean increase, 12 cells/year). The main characteristic common to these patients was the control of HIV replication. The HIV load was by definition nearly always 400 copies/mL during the follow-up period. Results of ultrasensitive tests with a lower limit of detection of 50 copies/mL revealed that 5 of 15 patients never had a detectable plasma HIV RNA load. The remaining 10 patients were found to have episodes of intermittent viremia (also known as “blips”): 38 (20%) of 178 virus load measurements were 150 copies/mL (median virus load, 165 copies/mL). For 2 patients, 1 (10%) of 10 and 1 (6.7%) of 15 virus load measurements were 1400 copies/mL.

The HIV DNA load in PBMCs was quantified (table 1). In all patients, the HIV DNA load in PBMCs was very low (mean HIV DNA load, 32 copies/106 PBMCs; range, 0–251 copies/106 PBMCs). Of interest, the 2 patients with the largest decrease in the CD4+ T cell count had higher HIV DNA levels in PBMCs. Of 7 patients from the SEROCO-HEMOCO cohort for whom sequential quantifications of HIV DNA were available, 6 had a stable HIV DNA load during the follow-up period. All patients in group A were infected with group M, subtype B HIV strains. We studied the immunological characteristics of patients in group A from whom fresh blood samples could be more easily obtained (table 1). Lymphoproliferative responses to p24 antigen were observed in all patients, with a mean stimulation index (SD) of and a mean net counts per minute 10.8 7 (SD) of. HIV-specific CD4+ T cells were 33,913 24,374 detected in 7 of 8 patients (mean SFC count, cells/622 715 106 PBMCs) and large numbers of HIV-specific CD8+ T cells