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Vaccinia virus uses macropinocytosis and apoptotic mimicry to enter host cells

Jason Mercer1, Ari Helenius

  • 1ETH Zurich, Institute of Biochemistry, Schafmattstrasse 18, ETH Hönggerberg HPM E6.3 Zurich, Switzerland.

Science (New York, N.Y.)
|April 26, 2008
PubMed

Insights

Vaccinia virus enters host cells using pH-dependent macropinocytosis, involving filopodia and membrane blebs. This process mimics apoptosis by utilizing exposed phosphatidylserine on the viral membrane for entry.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Viruses utilize diverse mechanisms for host cell entry.
  • Understanding viral entry pathways is crucial for developing antiviral strategies.

Purpose of the Study:

  • To elucidate the entry mechanism of vaccinia virus into host cells.
  • To investigate the role of specific cellular pathways and viral components in vaccinia virus infection.

Main Methods:

  • Live cell imaging of fluorescently labeled vaccinia virus particles.
  • Analysis of p21-activated kinase 1 (PAK1) activation.
  • Characterization of the endocytic process and its dependence on phosphatidylserine.

Main Results:

  • Vaccinia virus utilizes filopodia to reach the cell body and induces membrane blebs for internalization.
  • The entry process is pH-dependent and exhibits characteristics of macropinocytosis.
  • p21-activated kinase 1 (PAK1) is activated during viral entry.
  • Exposed phosphatidylserine on the viral membrane is essential for bleb induction, endocytosis, and infection.

Conclusions:

  • Vaccinia virus employs apoptotic mimicry, using exposed phosphatidylserine to facilitate entry via macropinocytosis.
  • The findings reveal a novel viral entry strategy involving membrane blebbing and filopodial trafficking.

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