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Human Parechovirus 1 Infection Occurs via αVβ1 Integrin

Pirjo Merilahti1, Sisko Tauriainen1, Petri Susi1

  • 1Department of Virology, University of Turku, Turku, Finland.

Plos One
|April 30, 2016
PubMed

Insights

Human parechovirus 1 (HPeV-1) uses the αVβ1 integrin for cellular entry, a key step in pediatric infections. This finding identifies a potential target for developing treatments against HPeV-1.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Human parechovirus 1 (HPeV-1) is a significant cause of pediatric respiratory and central nervous system infections globally.
  • Current treatments for HPeV-1 infections are lacking.
  • Previous studies suggested HPeV-1 binding to αVβ1, αVβ3, and αVβ6 integrins, but the specific cellular receptors for entry remained unidentified.

Purpose of the Study:

  • To identify the specific integrin receptors mediating infectious entry and replication of HPeV-1.
  • To analyze the expression profiles of integrins αVβ1, αVβ3, αVβ6, and α5β1 in susceptible cell lines.

Main Methods:

  • Antibody blocking assays were employed to inhibit integrin function.
  • Immunofluorescence microscopy was used to visualize receptor-virus interactions.
  • RT-qPCR was utilized to quantify gene expression levels.
  • Experiments involved susceptible cell lines (A549, HeLa, SW480), a β1-deficient mouse cell line (GE11-KO), and its β1-overexpressing derivative (GE11-β1).

Main Results:

  • HPeV-1 internalized and replicated in cell lines expressing αVβ1 integrin, but not in those expressing αVβ3 or αVβ6 integrins.
  • HPeV-1 failed to internalize into GE11-KO cells (lacking β1 integrin) but successfully entered GE11-β1 cells (overexpressing β1 integrin).
  • An integrin β1-activating antibody (TS2/16) enhanced HPeV-1 infectivity, and HPeV-1 co-localized and co-endocytosed with β1 integrin.

Conclusions:

  • The active form of αVβ1 integrin is the primary cellular receptor mediating the entry of HPeV-1 into susceptible cells.
  • HPeV-1 entry via αVβ1 integrin can occur without visible receptor clustering.
  • These findings identify αVβ1 integrin as a critical factor in HPeV-1 infection and a potential therapeutic target.

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