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Reovirus binding to cell surface sialic acid potentiates virus-induced apoptosis

J L Connolly1, E S Barton, T S Dermody

  • 1Departments of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Journal of Virology
|April 5, 2001
PubMed

Insights

Reovirus uses sialic acid binding via its sigma1 protein to efficiently induce apoptosis. Blocking this interaction prevents cell death, highlighting the role of viral attachment in apoptosis.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Reovirus is known to induce apoptosis (programmed cell death) in cells and living organisms.
  • The viral S1 gene, encoding attachment protein sigma1, dictates the efficiency of reovirus-induced apoptosis.
  • The specific biochemical properties of sigma1 influencing apoptosis remain unclear.

Purpose of the Study:

  • To investigate whether sigma1's ability to bind cell surface sialic acid influences the degree of apoptosis.
  • To elucidate the role of viral receptor engagement in reovirus-mediated cell death.

Main Methods:

  • Utilized isogenic reovirus mutants differing in sialic acid binding capacity.
  • Compared apoptosis induction levels in HeLa and L cells using sialic acid-binding (T3SA+) and non-binding (T3SA-) strains.
  • Assessed viral protein synthesis and progeny production to rule out these factors.
  • Enzymatically removed cell surface sialic acid using neuraminidase.
  • Blocked T3SA+ binding with sialyllactose.

Main Results:

  • T3SA+ induced high levels of apoptosis in both cell types, while T3SA- induced minimal to no apoptosis.
  • Apoptosis induction differences were not attributable to variations in viral protein synthesis or progeny production.
  • Neuraminidase treatment abolished T3SA+-induced apoptosis.
  • Sialyllactose incubation blocked T3SA+-induced apoptosis.

Conclusions:

  • Reovirus binding to cell surface sialic acid is essential for efficient apoptosis induction.
  • Virus-receptor interactions, specifically sigma1-sialic acid engagement, play a crucial role in regulating virus-induced cell death.
  • This suggests a broader mechanism where viral attachment strategies influence host cell fate.

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