AIM To evaluate alterations of memory B cell subpopulations during a 48-wk period in human immunodeficiency virus type 1(HIV-1) patients. METHODS Forty-one antiretroviral na?ve and 41 treated HIV-1 patients matched for age and duration of HIV infection were recruited. All clinical, epidemiological and laboratory data were recorded or measured. The different B cell subsets were characterized according to their surface markers: Total B cells(CD19~+), memory B cells(CD19~+CD27~+, BMCs), resting BMCs(CD19~+CD27~+CD21~(high), RM), exhausted BMCs(CD19~+CD21~(low)CD27-, EM), IgM memory B(CD19~+CD27~+IgM~(high)), isotype-switched BMCs(CD19~+CD27~+IgM-, ITS) and activated BMCs(CD19~+CD21~(low+)CD27~+, AM) at baseline on week 4 and week 48.RESULTS Mean counts of BMCs were higher in treated patients. There was a marginal upward trend of IgM memory B cell proportions which differed significantly in the treated group(overall trend, P = 0.004). ITS BMC increased over time significantly in all patients. Naive patients had of ~(low)er levels of EM B cells compared to treated, with a downward trend, irrespectively of ~(high)ly active antiretroviral therapy(HAART) intake. Severe impairment of EM B cells was recorded to both treated(P = 0.024) and naive(P = 0.023) and patients. Higher proportions of RM cells were noted in HAART group, which differed significantly on week 4~(th)(P = 0.017) and 48th(P = 0.03). Higher levels of AM were preserved in HAART naive group during the whole study period(week 4: P = 0.018 and 48: P = 0.035). HIV-RNA viremia strongly correlated with AM B cells(r = 0.54, P = 0.01) and moderately with RM cells(r =-0.45, P = 0.026) at baseline.CONCLUSION HIV disrupts memory B cell subpopulations leading to impaired immunologic memory over time. BMC, RM, EM and ITS BMC were higher in patients under HAART. Activated BMCs(AM) were higher in patients without HAART. Viremia correlated with AM and RM. Significant depletion was recorded in EM B cells irrespectively of HAART intake. Perturbations in BMC-populations are not fully restored by antiretrovirals. AIM To evaluate alterations of memory B cell subpopulations during a 48-wk period in human immunodeficiency virus type 1 (HIV-1) patients. METHODS Forty-one antiretroviral naïve and 41 treated HIV-1 patients matched for age and duration of HIV All clinical, epidemiological and laboratory data were recorded or measured. The different B cell subsets were characterized according to their surface markers: Total B cells (CD19 ~ +), memory B cells (CD19 ~ + CD27 ~ +, BMCs ), resting BMCs (CD19 + CD27 + CD21 high, RM), exhausted BMCs (CD19 + CD21 low CD27-, EM), IgM memory B (CD19 ~ + CD27 ~ + IgM-, ITS) and activated BMCs (CD19 ~ + CD21 ~ (low +) CD27 ~ +, AM) at baseline on week 4 and week 48.RESULTS Mean counts of was BMCs were higher in treated patients. There was a marginal upward trend of IgM memory B cell proportions which differed significantly in the treated group (overall trend, P = 0.004). ITS BMC increased over time significantly in all patien ts. Naive patients had of low levels of EM B cells compared to treated, with a downward trend, irrespectively of ~ (high) ly active antiretroviral therapy (HAART) intake. Severe impairment of EM B cells was recorded to both Higher proportions of RM cells were noted in the HAART group, which differed significantly from week 4 th (P = 0.017) and 48 th (P = 0.03). High levels of AM were preserved in HAART naive group during the whole study period (week 4: P = 0.018 and 48: P = 0.035). HIV-RNA viremia strongly correlated with AM B cells Medianly with RM cells (r = -0.45, P = 0.026) at baseline. CONCLUSION HIV disrupts memory B cell subpopulations leading to impaired immunologic memory over time. BMC, RM, EM and ITS BMC were higher in patients under HAART. Activated BMCs ( AM) were higher in patients without HAART. Viremia correlated with AM and RM. Significant depletion was recorded in EM B cells irrespectively of HAARTintake. Perturbations in BMC-populations are not fully restored by antiretrovirals.