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Modification of cellular autophagy protein LC3 by poliovirus

Matthew P Taylor1, Karla Kirkegaard

  • 1Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.

Journal of Virology
|September 7, 2007
PubMed

Insights

Poliovirus infection hijacks cellular autophagy, modifying the host protein LC3 early in the process. However, double-membraned vesicle formation requires additional viral proteins, suggesting targeted subversion of innate immunity.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Poliovirus infection induces intracellular membrane remodeling for viral RNA replication.
  • Poliovirus-induced vesicles share characteristics with cellular autophagosomes, including LAMP-1 acquisition and LC3 recruitment.
  • Autophagy involves LC3 lipidation, a marker for autophagosome formation and membrane association.

Purpose of the Study:

  • To investigate the role of poliovirus proteins in LC3 modification and autophagosome-like vesicle formation.
  • To determine if early steps of autophagy, like LC3 modification, can be separated from later steps.
  • To understand how poliovirus subverts the innate immune response through autophagy manipulation.

Main Methods:

  • Analysis of LC3 modification during poliovirus infection.
  • Expression of the viral protein 2BC to assess its role in LC3 modification.
  • Investigating the requirement of viral proteins 2BC and 3A for double-membraned vesicle formation.

Main Results:

  • Poliovirus infection and expression of viral protein 2BC induce LC3 modification, similar to autophagy.
  • LC3 modification can be genetically separated from the induction of double-membraned vesicles.
  • Formation of these vesicles requires both viral proteins 2BC and 3A.

Conclusions:

  • Poliovirus selectively induces early autophagy steps (LC3 modification) via protein 2BC.
  • Later steps, including double-membraned vesicle formation, require additional viral proteins (2BC and 3A).
  • This suggests poliovirus directly subverts a specific branch of the innate immune response.

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