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Unstable receptors disappear from cell surface during poliovirus infection.

Nickolay Neznanov, Konstantin P. Chumakov, Axel Ullrich, Vadim I. Agol, Andrei V. Gudkov

Med Sci Monit 2002; 8(10): BR391-396

ID: 4879

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. MATERIAL/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.

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