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09:27

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Apoptotic mimicry: phosphatidylserine-mediated macropinocytosis of vaccinia virus

Jason Mercer1, Ari Helenius

  • 1ETH Zurich, Institute of Biochemistry, Zurich, Switzerland. jason.mercer@bc.biol.ethz.ch

Annals of the New York Academy of Sciences
|October 21, 2010
PubMed

Insights

Vaccinia virus enters host cells using macropinocytosis, a process triggered by phosphatidylserine on the virus membrane. This mechanism mimics apoptotic bodies, involving actin network changes and membrane blebbing for viral entry.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Viruses are obligate intracellular parasites dependent on host cell machinery.
  • Most viruses utilize cellular endocytosis for entry into host cells.
  • Vaccinia virus, a poxvirus, has recently been shown to employ macropinocytosis for cell entry.

Purpose of the Study:

  • To investigate the mechanism of vaccinia virus entry into host cells.
  • To elucidate the role of cellular processes in vaccinia virus infection.
  • To understand the signaling pathways involved in vaccinia virus-induced macropinocytosis.

Main Methods:

  • Analysis of vaccinia virus entry pathways.
  • Investigation of cellular signaling networks activated by virus entry.
  • Examination of the cortical actin network dynamics during infection.
  • Assessment of the role of phosphatidylserine in viral entry.

Main Results:

  • Vaccinia virus utilizes macropinocytosis for cellular entry.
  • Viral entry triggers a signaling cascade leading to cortical actin rearrangement.
  • Membrane blebbing, a characteristic of macropinocytosis, facilitates virus internalization.
  • Phosphatidylserine on the virus membrane is essential for initiating signaling, blebbing, and macropinocytosis.

Conclusions:

  • Vaccinia virus employs a unique entry strategy involving macropinocytosis.
  • The virus mimics apoptotic bodies by utilizing phosphatidylserine to trigger host cell entry mechanisms.
  • Understanding this entry mechanism provides insights into viral pathogenesis and host-pathogen interactions.

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