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Virus-ligand interactions of OC43 coronavirus with cell membranes

A R Collins1

  • 1Department of Microbiology, State Univ. of NY at Buffalo 14214.

Insights

Human coronavirus OC43 binds to two receptors on susceptible cells: a 90 kD glycoprotein and HLA class I antigen. Antibodies targeting these receptors reduce virus yield, suggesting potential therapeutic targets.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Human coronavirus OC43 (HCoV-OC43) is a significant respiratory pathogen.
  • Understanding virus-receptor interactions is crucial for developing antiviral strategies.
  • Rhabdomyosarcoma (RD) cells are highly susceptible to HCoV-OC43 infection.

Purpose of the Study:

  • To identify and characterize the cellular receptors for HCoV-OC43 on RD cells.
  • To investigate the role of these receptors in viral entry and infection.
  • To explore the potential of receptor blockade as an antiviral approach.

Main Methods:

  • Solid phase virus binding assays were employed to detect virus-receptor interactions.
  • Receptor blockade assays were used to assess the functional role of identified receptors.
  • Neuraminidase and NaOH treatments were utilized to confirm receptor specificity.

Main Results:

  • HCoV-OC43 virions and spike proteins bound to a 90 kD glycoprotein on RD cells, resistant to enzymatic and chemical treatments.
  • A 45 kD receptor, identified as HLA class I antigen, also mediated virus binding.
  • Antibodies against both the 90 kD glycoprotein and HLA class I antigen reduced virus yield.
  • Serum from multiple sclerosis patients showed blocking activity correlated with anti-HLA antibodies, but not anti-90 kD glycoprotein antibodies.

Conclusions:

  • HCoV-OC43 utilizes a 90 kD glycoprotein and HLA class I antigen as cellular receptors on RD cells.
  • Both receptors play a role in viral infection, as evidenced by antibody-mediated reduction in virus yield.
  • The presence of anti-HLA antibodies in multiple sclerosis patients suggests a potential link between HLA and coronavirus infection, warranting further investigation.

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