title: Unstable receptors disappear from cell surface during poliovirus infection.
abstract: BACKGROUND
  Cellular receptors play a significant role in pathogenesis of viral infections. Previously, we demonstrated that TNFa receptor (TNFR1) rapidly disappeared from the cell surface upon poliovirus infection, whereas FAS was much more stable [1]. We suggested that the rate of decrease in receptor presentation on the surface of infected cells might reflect its turnover rate on uninfected cells.
  
  
  METHODS
  To test this hypothesis, we estimated by FACS analysis the turnover rates of receptors for TRAIL (TRAILR1 and TRAILR2), signal regulatory protein SIRPa, receptor for alpha/beta interferon (INFR1), and poliovirus receptor (CD155) on the surface of HeLa cells after the treatment with brefeldin A (to stop receptor replenishment through the Golgi-mediated trafficking) or poliovirus infection.
  
  
  RESULTS
  A good correlation between turnover rates caused by the two interventions was observed, with the stability of receptor presentation changing in the following order: TRAILR1, TRAILR2, SIRPa (half-life on infected cells between 2-4 h) < INFR1 (4-6 h) < CD155 (>8 h, besides some early masking of the receptor by its binding of the virus).
  
  
  CONCLUSIONS
  Our results suggest that disruption of the protein trafficking pathway during poliovirus infection leads to the diminished sensitivity of infected cells to pro-apoptotic factors, and thus represents one of the mechanisms by which virus modulates the host defense reactions.
authors.affiliation: Department of Virology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. neznann@ccf.org
authors.forename: Nickolay
authors.initials: N
authors.lastname: Neznanov
authors.forename: Konstantin P
authors.initials: KP
authors.lastname: Chumakov
authors.forename: Axel
authors.initials: A
authors.lastname: Ullrich
authors.forename: Vadim I
authors.initials: VI
authors.lastname: Agol
authors.forename: Andrei V
authors.initials: AV
authors.lastname: Gudkov
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D020126:Brefeldin A / Q000378:metabolism; D002460:Cell Line; D002469:Cell Separation; D005434:Flow Cytometry; D006367:HeLa Cells; D006801:Humans; D008565:Membrane Proteins; D011051:Poliomyelitis / Q000378:metabolism*; D017955:Poliovirus / Q000378:metabolism*; D011500:Protein Synthesis Inhibitors / Q000378:metabolism; D021381:Protein Transport / Q000502:physiology; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D011991:Receptors, Virus / Q000378:metabolism*
chemical_list: D008565:Membrane Proteins; D011500:Protein Synthesis Inhibitors; D018124:Receptors, Tumor Necrosis Factor; D011991:Receptors, Virus; C066100:poliovirus receptor; D020126:Brefeldin A