Vaccinia Virus Uses Macropinocytosis and Apoptotic Mimicry to Enter Host Cells

  title={Vaccinia Virus Uses Macropinocytosis and Apoptotic Mimicry to Enter Host Cells},
  author={Jason Mercer and Ari Helenius},
  pages={531 - 535}
Viruses employ many different strategies to enter host cells. Vaccinia virus, a prototype poxvirus, enters cells in a pH-dependent fashion. Live cell imaging showed that fluorescent virus particles associated with and moved along filopodia to the cell body, where they were internalized after inducing the extrusion of large transient membrane blebs. p21-activated kinase 1 (PAK1) was activated by the virus, and the endocytic process had the general characteristics of macropinocytosis. The… 

Cellular microbiology: Virus plays dead

  • A. Heinrichs
  • Biology
    Nature Reviews Molecular Cell Biology
  • 2008
Viral PS might be analogous to cellular PS and triggers the uptake of virus particles by mimicking apoptotic bodies and late-stage vaccinia-infected cells were shown to undergo apoptosis, indicating that blebbing is required for infection.

Poxvirus host cell entry.

Virus Entry by Endocytosis

This review focuses on the cell biology of virus entry and the different strategies and endocytic mechanisms used by animal viruses.

Late-penetrating viruses.

Enveloped RNA virus utilization of phosphatidylserine receptors: Advantages of exploiting a conserved, widely available mechanism of entry

For viruses that use their glycans and/or lipids as attachment/internalization factors, additional entry steps, such as binding within the endosomal compartment to a cellular receptor that stimulates fusion events, are required for productive infection.

Acrylamide Inhibits Vaccinia Virus Through Vimentin-independent Anti-Viral Granule Formation

It is concluded that vimentin is dispensable for poxvirus replication and assembly and that acrylamide, as a potent inducer of AVGs during VACV infection, serves to bolster cell’s antiviral response to poXvirus infection.



Vaccinia Virus Entry into Cells via a Low-pH-Dependent Endosomal Pathway

It is demonstrated that entry of mature vaccinia virions is accelerated by brief low-pH treatment and severely reduced by inhibitors of endosomal acidification, providing evidence for a predominant low- pH-dependent endosome pathway.

Influenza Virus Can Enter and Infect Cells in the Absence of Clathrin-Mediated Endocytosis

It is demonstrated that influenza virus may enter and infect HeLa cells that are unable to take up ligands by clathrin-mediated endocytosis, and is believed to be the first conclusive analysis of virus entry via such a non-clathrin -dependent, non-caveola-dependent endocytic pathway.

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Apoptotic cell removal

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It is shown that the vaccinia F11L protein interacts directly with RhoA, inhibiting its signaling by blocking the interaction with its downstream effectors Rho-associated kinase (ROCK) and mDia.

Listeria hijacks the clathrin-dependent endocytic machinery to invade mammalian cells

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Actin- and myosin-driven movement of viruses along filopodia precedes their entry into cells

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By using electron microscopy, it is demonstrated that IMV from strains Western Reserve and modified virus Ankara enter cells by fusion with the plasma membrane and enters by fusion at the cell surface.