title: Cultured Kaposi's sarcoma tumor cells exhibit a chemokine receptor repertoire that does not allow infection by HIV-1.
abstract: BACKGROUND
  HIV-1 is known to play a critical role in the pathogenesis of AIDS-associated Kaposi's sarcoma (KS). However, it remains controversial whether KS cells are target cells for HIV infection. The aim of this study was to investigate the expression of chemokine receptors in KS cell cultures and to determine whether these cells can be infected by HIV-1.
  
  
  METHODS
  KS-derived cells and KS-Y1 cells were investigated using RT-PCR for the expression of CD4, CCR3, CCR5, CCR8 and CXCR4 mRNA. HIV infectivity of these cells was determined by p24 antigen and HIV-1 RNA production, as well as by HIV-1 DNA integration.
  
  
  CONCLUSIONS
  With the exception of CCR8 which is expressed by KS-derived spindle cell cultures but not by KS-Y1 cells, unstimulated KS cells express no significant levels of CD4, CCR3, CCR5 or CXCR4 mRNA. HIV infectivity assays showed that KS cells were unpermissive to HTLVIIIB and JRFL strains. Although the expression of CXCR4 mRNA could be upregulated by interleukin-1beta, stimulation of KS cells by this cytokine did not allow infection by HIV-1.
  
  
  CONCLUSIONS
  This shows that KS cells exhibit a chemokine receptor repertoire that does not allow infection by HIV-1. Other cell types making up KS lesions, such as inflammatory cells, are likely to represent the source of HIV-1 products cooperating to promote KS development and progression.
authors.affiliation: Department of Dermatology, Erasme University Hospital, 808 Route de Lennick, Brussels, 1070, Belgium. tsimonar@ulb.ac.be
authors.forename: T
authors.initials: T
authors.lastname: Simonart
authors.forename: C
authors.initials: C
authors.lastname: Debussher
authors.forename: C
authors.initials: C
authors.lastname: Liesnard
authors.forename: L
authors.initials: L
authors.lastname: Debaisieux
authors.forename: M L
authors.initials: ML
authors.lastname: Delforge
authors.forename: A
authors.initials: A
authors.lastname: de Lavareille
authors.forename: P
authors.initials: P
authors.lastname: Hermans
authors.forename: J P
authors.initials: JP
authors.lastname: Van Vooren
authors.forename: P
authors.initials: P
authors.lastname: Stordeur
mesh_terms: D000199:Actins / Q000378:metabolism; D015704:CD4 Antigens / Q000378:metabolism; D004279:DNA, Viral / Q000302:isolation & purification; D018450:Disease Progression; D015497:HIV-1 / Q000235:genetics / Q000302:isolation & purification* / Q000472:pathogenicity*; D006801:Humans; D012333:RNA, Messenger / Q000032:analysis; D012367:RNA, Viral / Q000302:isolation & purification; D054397:Receptors, CCR3; D019713:Receptors, CCR5 / Q000378:metabolism; D054401:Receptors, CCR8; D019718:Receptors, CXCR4 / Q000235:genetics / Q000378:metabolism; D019707:Receptors, Chemokine / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012514:Sarcoma, Kaposi / Q000378:metabolism* / Q000821:virology*; D014407:Tumor Cells, Cultured / Q000378:metabolism / Q000821:virology
chemical_list: D000199:Actins; C515350:CCR3 protein, human; C103330:CCR8 protein, human; D015704:CD4 Antigens; D004279:DNA, Viral; D012333:RNA, Messenger; D012367:RNA, Viral; D054397:Receptors, CCR3; D019713:Receptors, CCR5; D054401:Receptors, CCR8; D019718:Receptors, CXCR4; D019707:Receptors, Chemokine