title: Higher SLPI expression, lower immune activation, and increased frequency of immune cells in a cohort of Colombian HIV-1 controllers.
abstract: BACKGROUND
  There are 2 new phenotypes of HIV-1-positive individuals who exhibit a spontaneous and sustained control of viral replication at least for 1 year without antiretroviral therapy (elite controllers <50 copies/mL and viremic controllers <2000 copies/mL). Mechanisms related to this spontaneous control of viral replication are poorly understood.
  
  
  METHODS
  The study included HIV-1 controllers (patients with at least 1 year of HIV-1 diagnosis, highly active antiretroviral therapy naive, and with viral loads less than 2000 copies/mL) and HIV-1 progressors without antiretroviral therapy (viral load >2500 copies/mL, and CD4 T-cell count >250 cells/μL at the time of sampling). The expression of soluble factors, leukocyte protease inhibitor (SLPI) and human α-defensins-1 (HAD-1), was measured by real-time polymerase chain reaction from neutrophil cultures with or without HIV stimulation; the frequency and phenotype of innate and adaptive immune cells were determined by flow cytometry, and frequency of human leukocyte antigen alleles was determined by polymerase chain reaction sequence-specific oligonucleotide typing.
  
  
  RESULTS
  As expected, HIV-1 controllers had higher CD4 T-cell counts and lower viral load when compared with HIV-1 progressor individuals; in addition, they exhibited lower expression of activation markers, higher frequency of myeloid dendritic cell, lower percentage of regulatory T cells and natural killer cells, and higher expression of SLPI.
  
  
  CONCLUSIONS
  All together, these findings suggest that the control of the immune activation status and the production of antiviral proteins by innate immune cells could be associated to the mechanisms involved in the control of HIV-1 replication and better preservation of the CD4 T-cell count.
authors.affiliation: Immunovirology Group, School of Medicine, Universidad de Antioquia, Medellin, Colombia.
authors.forename: Natalia A
authors.initials: NA
authors.lastname: Taborda
authors.forename: Juan C
authors.initials: JC
authors.lastname: Cataño
authors.forename: Julio C
authors.initials: JC
authors.lastname: Delgado
authors.forename: María T
authors.initials: MT
authors.lastname: Rugeles
authors.forename: Carlos J
authors.initials: CJ
authors.lastname: Montoya
mesh_terms: D000328:Adult; D000483:Alleles; D002478:Cells, Cultured; D003105:Colombia; D005260:Female; D005434:Flow Cytometry; D020869:Gene Expression Profiling; D015658:HIV Infections / Q000276:immunology* / Q000821:virology; D020276:HIV Long-Term Survivors; D015497:HIV-1 / Q000276:immunology* / Q000302:isolation & purification; D006680:HLA Antigens / Q000032:analysis / Q000235:genetics; D006801:Humans; D007113:Immunity, Innate; D016130:Immunophenotyping; D007962:Leukocytes / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D060888:Real-Time Polymerase Chain Reaction; D053481:Secretory Leukocyte Peptidase Inhibitor / Q000096:biosynthesis*; D019562:Viral Load; D023084:alpha-Defensins / Q000096:biosynthesis
chemical_list: D006680:HLA Antigens; C506814:SLPI protein, human; D053481:Secretory Leukocyte Peptidase Inhibitor; D023084:alpha-Defensins