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Tyro3 family-mediated cell entry of Ebola and Marburg viruses

Masayuki Shimojima1, Ayato Takada, Hideki Ebihara

  • 1Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.

Journal of Virology
|September 29, 2006
PubMed

Insights

Filoviruses, like Ebola and Marburg viruses, use Tyro3 receptor tyrosine kinases (Axl, Dtk, Mer) for cell entry. These receptors enhance filovirus infection, revealing a key mechanism for their broad tissue tropism.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Mechanisms

Background:

  • Filoviruses (Ebolavirus, Marburgvirus) cause severe hemorrhagic fever.
  • The molecular basis for filovirus broad tissue tropism is not well understood.

Purpose of the Study:

  • To investigate the role of Tyro3 receptor tyrosine kinase family members in filovirus cell entry.
  • To identify molecular factors contributing to filovirus broad tropism.

Main Methods:

  • Ectopic expression of Tyro3 family members (Axl, Dtk, Mer) in lymphoid cells.
  • Infection assays using filovirus pseudotype viruses and live Ebola virus.
  • Inhibition studies using antibodies and soluble ectodomains of Tyro3 family members.

Main Results:

  • Ectopic expression of Axl, Dtk, and Mer enhanced filovirus pseudotype virus infection in lymphoid cells.
  • Infection enhancement was reduced by antibodies to Tyro3 family members or their ligand Gas6.
  • Live Ebola virus infected Axl- and Dtk-expressing cells more efficiently.
  • Antibody to Axl inhibited pseudotype virus infection in Axl-positive cell lines.

Conclusions:

  • Members of the Tyro3 receptor tyrosine kinase family (Axl, Dtk, Mer) are involved in filovirus cell entry.
  • These receptors act as cell entry factors, contributing to the broad tropism of filoviruses.

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