title: Downregulation of Cytokines and Chemokines by GB Virus C After Transmission Via Blood Transfusion in HIV-Positive Blood Recipients.
abstract: BACKGROUND
  An association between GB virus C (GBV-C) and improved outcomes of human immunodeficiency virus (HIV) infection has been reported in HIV-positive individuals with active GBV-C coinfection. This study provides insights into the immune mechanisms underlying the protective role of GBV-C in HIV-infected patients.
  
  
  METHODS
  The concentrations of 64 cytokines and chemokines were measured in plasma samples obtained from the Viral Activation Transfusion Study cohort before transfusion and longitudinally from 30 patients positive for both HIV and GBV-C (hereafter, "cases") and 30 patients positive for HIV and negative for GBV-C (hereafter, "controls").
  
  
  RESULTS
  Cases had lower HIV viral loads and higher CD4 T-cell counts than controls after acquisition of GBV-C infection. Most of the modulated cytokines and chemokines were reduced after GBV-C detection, including many proinflammatory cytokines, suggesting an overall antiinflammatory effect of GBV-C in HIV-positive subjects. Most pathways and functions of the measured cytokines were downregulated in cases, except cell death pathways, which were upregulated in various cell subsets in the 3 months after GBV-C detection.
  
  
  CONCLUSIONS
  GBV-C has a protective effect, in part through a competition mechanism leading to decreased inflammation and improved HIV disease outcome in cases. Further studies are necessary to establish whether GBV-C may have deleterious effects on the host at the cellular level, including depleting the cells that are the targets of HIV.
authors.affiliation: Blood Systems Research Institute.
authors.forename: Marion C
authors.initials: MC
authors.lastname: Lanteri
authors.affiliation: Blood Systems Research Institute.
authors.forename: Farnaz
authors.initials: F
authors.lastname: Vahidnia
authors.affiliation: RTI International, Rockville, Maryland.
authors.forename: Sylvia
authors.initials: S
authors.lastname: Tan
authors.affiliation: Iowa City Veterans Affairs Hospital University of Iowa Carver College of Medicine, Iowa City.
authors.forename: Jack T
authors.initials: JT
authors.lastname: Stapleton
authors.affiliation: Blood Systems Research Institute Department of Laboratory Medicine Department of Medicine, University of California-San Francisco, California.
authors.forename: Philip J
authors.initials: PJ
authors.lastname: Norris
authors.affiliation: Blood Systems Research Institute.
authors.forename: John
authors.initials: J
authors.lastname: Heitman
authors.affiliation: Blood Systems Research Institute.
authors.forename: Xutao
authors.initials: X
authors.lastname: Deng
authors.affiliation: Blood Systems Research Institute.
authors.forename: Sheila M
authors.initials: SM
authors.lastname: Keating
authors.affiliation: RTI International, Rockville, Maryland.
authors.forename: Don
authors.initials: D
authors.lastname: Brambilla
authors.affiliation: Blood Systems Research Institute Department of Laboratory Medicine.
authors.forename: Michael P
authors.initials: MP
authors.lastname: Busch
authors.affiliation: Blood Systems Research Institute Department of Laboratory Medicine.
authors.forename: Brian
authors.initials: B
authors.lastname: Custer
mesh_terms: D000328:Adult; D001803:Blood Transfusion; D016207:Cytokines / Q000097:blood*; D015536:Down-Regulation; D005260:Female; D018178:Flaviviridae Infections / Q000276:immunology* / Q000821:virology; D029407:GB virus C / Q000502:physiology*; D015658:HIV Infections / Q000150:complications* / Q000473:pathology*; D006525:Hepatitis, Viral, Human / Q000276:immunology* / Q000821:virology; D006801:Humans; D007249:Inflammation / Q000473:pathology; D008297:Male
chemical_list: D016207:Cytokines
keywords: GBV-C; HIV coinfection; HIV disease outcome; HIV disease progression markers; cytokine and chemokine responses; transfusion-transmission