title: Increased frequency of CD27- (naive) B cells and their phenotypic alteration in HIV type 1-infected patients.
abstract: To investigate HIV-1-related B cell disorders, the quantity of peripheral CD27 negative (CD27-) B cells, their CD38, CD95, and bcl-2 intensities, and their apoptosis susceptibility were examined by flow cytometry analysis in 16 drug-naive patients, 27 HAART-treated patients, and 20 uninfected controls. CD27- B cells have been recognized as naive B cells. The mean percentage of CD27- B cells was significantly higher in drugnaive patients (88.1%) and in HAART-treated patients (83.9%) than in controls (68.6%) (p < 0.01). The intensities of CD38 and CD95 on CD27- B cells were significantly higher in drug-naive patients than in controls (p < 0.01). The intensity of CD95 on CD27- B cells in HAART-treated patients was lower than that of drug-naive patients, but significantly higher than that of controls (p < 0.01). The intensity of bcl-2 on CD27- B cells in drug-naive patients was lower than that of controls. In drug-naive patients, CD27-B cells with high CD38 expression represented low bcl-2 expression. The CD27- B cells of drug-naive patients showed an increased susceptibility to apoptosis, characterized by diminished cell size and a high frequency of annexin-V binding, compared with controls and HAART-treated patients. These findings suggested that HIV-1 infection affects peripheral CD27- (naive) B cells as well as CD27+ (memory) B cells and that CD27- B cells might be activated and rendered highly susceptible to apoptosis by HIV-1 infection. Some phenotypic alterations in CD27- B cells may continue after the reduction of HIV-1 loads by effective antiviral therapy.
authors.affiliation: Department of General Medicine, Kyushu University, Fukuoka 812-8582, Japan.
authors.forename: Yong
authors.initials: Y
authors.lastname: Chong
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Ikematsu
authors.forename: Masahiro
authors.initials: M
authors.lastname: Yamamoto
authors.forename: Masayuki
authors.initials: M
authors.lastname: Murata
authors.forename: Kouzaburo
authors.initials: K
authors.lastname: Yamaji
authors.forename: Mika
authors.initials: M
authors.lastname: Nishimura
authors.forename: Shigeki
authors.initials: S
authors.lastname: Nabeshima
authors.forename: Seizaburo
authors.initials: S
authors.lastname: Kashiwagi
authors.forename: Jun
authors.initials: J
authors.lastname: Hayashi
mesh_terms: D036541:ADP-ribosyl Cyclase / Q000032:analysis; D051997:ADP-ribosyl Cyclase 1; D000328:Adult; D017304:Annexin A5 / Q000378:metabolism; D019380:Anti-HIV Agents / Q000627:therapeutic use; D015703:Antigens, CD / Q000032:analysis; D023241:Antiretroviral Therapy, Highly Active; D017209:Apoptosis; D016175:B-Lymphocyte Subsets / Q000276:immunology* / Q000502:physiology; D005434:Flow Cytometry; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D015497:HIV-1; D006801:Humans; D016130:Immunophenotyping; D018655:Lymphocyte Count; D008562:Membrane Glycoproteins; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D013194:Staining and Labeling; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7 / Q000032:analysis*; D019014:fas Receptor / Q000032:analysis
chemical_list: D017304:Annexin A5; D019380:Anti-HIV Agents; D015703:Antigens, CD; D008562:Membrane Glycoproteins; D019253:Proto-Oncogene Proteins c-bcl-2; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7; D019014:fas Receptor; D036541:ADP-ribosyl Cyclase; C498154:CD38 protein, human; D051997:ADP-ribosyl Cyclase 1