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Caveolar endocytosis is required for human PSGL-1-mediated enterovirus 71 infection

Hsiang-Yin Lin1, Ya-Ting Yang, Shu-Ling Yu

  • 1Institute of Infectious Disease and Vaccinology, National Health Research Institutes, Zhunan, Miaoli County, Taiwan.

Journal of Virology
|June 14, 2013
PubMed

Insights

Enterovirus 71 (EV71) uses different entry pathways depending on the cell receptor. P-selectin glycoprotein ligand-1 (PSGL-1) mediates entry via caveola-dependent endocytosis, while human scavenger receptor class B member 2 (hSCARB2) uses clathrin-dependent endocytosis.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Mechanisms

Background:

  • Enterovirus 71 (EV71) is a significant pathogen causing hand, foot, and mouth disease and severe neurological complications in children.
  • Human scavenger receptor class B member 2 (hSCARB2) and P-selectin glycoprotein ligand-1 (PSGL-1) are known receptors for EV71.
  • The precise mechanism of EV71 entry mediated by PSGL-1 is not fully understood.

Purpose of the Study:

  • To elucidate the endocytic pathways utilized by EV71 for cellular entry.
  • To differentiate the roles of PSGL-1 and hSCARB2 in EV71-mediated endocytosis.
  • To investigate the cellular mechanisms governing EV71 infection.

Main Methods:

  • Investigated EV71 entry in Jurkat T cells, PSGL-1-expressing L929 cells (PSGL-1-L929), and hSCARB2-expressing RD cells.
  • Utilized specific endocytosis inhibitors and siRNA targeting caveolin-1 to block clathrin- and caveola-dependent pathways.
  • Employed confocal immunofluorescence to visualize the colocalization of EV71 with cellular structures.

Main Results:

  • Clathrin-dependent endocytosis was essential for EV71 infection in RD cells (hSCARB2-mediated) but not in Jurkat T or PSGL-1-L929 cells.
  • Caveola-dependent endocytosis was critical for EV71 infection in Jurkat T and PSGL-1-L929 cells, with direct colocalization observed between EV71 and caveolae.
  • EV71 infection was dependent on pH-mediated endosomal acidification and intact membrane cholesterol.

Conclusions:

  • EV71 employs distinct endocytic routes dependent on the cellular receptor.
  • PSGL-1 facilitates EV71 entry through a caveola-dependent mechanism.
  • hSCARB2 mediates EV71 entry via clathrin-dependent endocytosis, highlighting receptor-specific internalization pathways.

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