title: Increased platelet and microparticle activation in HIV infection: upregulation of P-selectin and tissue factor expression.
abstract: OBJECTIVE
  HIV-1-infected patients have an increased risk for atherothrombosis and cardiovascular disease, but the mechanism behind these risks is poorly understood. We have previously reported that expression of tissue factor (TF) on circulating monocytes is increased in persons with HIV infection and that TF expression is related to immune activation, to levels of HIV in plasma, and to indices of microbial translocation. In this study, we explore the activation state of platelets in HIV disease.
  
  
  METHODS
  Here, using flow cytometry-based assays, we measured platelet and platelet microparticle (PMP) activation in samples from HIV-1-infected donors and controls.
  
  
  RESULTS
  Platelets and PMPs from HIV-1-infected patients are activated (as reflected by expression of CD62 P-selectin) and also more frequently expressed the procoagulant TF than did platelets and PMPs obtained from controls. Expression of these proteins was directly related to expression of TF on monocytes, to markers of T-cell activation (CD38 and HLA-DR), and to plasma levels of soluble CD14, the coreceptor for bacterial lipopolysaccharride. Platelet and microparticle expression of TF was not related to plasma levels of HIV but expression of P-selectin was related to plasma levels of HIV; neither TF nor P-selectin expression was related to CD4 T-cell count.
  
  
  CONCLUSIONS
  Platelets and microparticles are activated in HIV infection, and this activated phenotype may contribute to the increased risk for cardiovascular and thrombotic events in this population although a role for other confounding cardiovascular risks cannot be completely excluded.
authors.affiliation: National Health Laboratory Services and University of Witwatersrand, Johannesburg, South Africa.
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Mayne
authors.forename: Nicholas T
authors.initials: NT
authors.lastname: Funderburg
authors.forename: Scott F
authors.initials: SF
authors.lastname: Sieg
authors.forename: Robert
authors.initials: R
authors.lastname: Asaad
authors.forename: Magdalena
authors.initials: M
authors.lastname: Kalinowska
authors.forename: Benigno
authors.initials: B
authors.lastname: Rodriguez
authors.forename: Alvin H
authors.initials: AH
authors.lastname: Schmaier
authors.forename: Wendy
authors.initials: W
authors.lastname: Stevens
authors.forename: Michael M
authors.initials: MM
authors.lastname: Lederman
mesh_terms: D051997:ADP-ribosyl Cyclase 1 / Q000096:biosynthesis; D000328:Adult; D000368:Aged; D001792:Blood Platelets / Q000821:virology*; D018791:CD4 Lymphocyte Count; D055252:Cell-Derived Microparticles / Q000821:virology*; D005260:Female; D005434:Flow Cytometry; D015658:HIV Infections / Q000378:metabolism*; D006684:HLA-DR Antigens / Q000096:biosynthesis; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000097:blood; D008213:Lymphocyte Activation; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D019007:P-Selectin / Q000096:biosynthesis*; D015539:Platelet Activation; D013925:Thromboplastin / Q000096:biosynthesis*; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D006684:HLA-DR Antigens; D018950:Lipopolysaccharide Receptors; D008562:Membrane Glycoproteins; D019007:P-Selectin; D013925:Thromboplastin; C498154:CD38 protein, human; D051997:ADP-ribosyl Cyclase 1