Unstable Receptors Disappear from Cell Surface During Poliovirus Infection

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.