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High permissivity of human HepG2 hepatoma cells for influenza viruses

Laurence Ollier1, Anne Caramella, Valérie Giordanengo

  • 1INSERM U526-Laboratoire de Virologie, Faculté de Médecine, avenue de Valombrose, 06107 Nice cedex 2, France. lefebvre@unice.fr.

Journal of Clinical Microbiology
|December 8, 2004
PubMed

Insights

HepG2 cells efficiently support influenza virus replication, aiding primary isolation. Tranexamic acid inhibited virus growth, suggesting a role for plasminogen activators in influenza virus infection.

Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Human HepG2 hepatoma cells are susceptible to influenza A and B viruses.
  • These cells show a significant cytopathic effect, facilitating virus isolation.
  • The role of cell surface proteases in influenza virus replication is not fully understood.

Purpose of the Study:

  • To investigate the permissiveness of HepG2 cells for influenza virus isolation.
  • To explore the potential involvement of the plasminogen/tissue plasminogen activator (t-PA) complex in influenza virus replication in HepG2 cells.

Main Methods:

  • Infection of HepG2 cells with influenza virus types A and B.
  • Observation of cytopathic effects.
  • Treatment with tranexamic acid, a plasmin(ogen)-specific inhibitor.
  • Assessment of virus replication levels.

Main Results:

  • HepG2 cells demonstrated high permissiveness for both influenza A and B viruses without trypsin.
  • A marked cytopathic effect was observed in infected HepG2 cells.
  • Tranexamic acid significantly reduced influenza virus replication.
  • This suggests a role for the cell surface plasminogen/t-PA complex in supporting influenza virus replication.

Conclusions:

  • HepG2 cells are a valuable model for influenza virus primary isolation.
  • The plasminogen/t-PA system on HepG2 cell surfaces may play a role in influenza virus replication.
  • This finding opens new avenues for studying host-virus interactions involving plasminogen activators.

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