title: Viruses and arrested autophagosome development.
abstract: Autophagy is acknowledged as an important cellular defense mechanism against intracellular pathogens. As with other innate immune responses, pathogens have adapted to evade autophagy and in some cases, subvert the pathway to promote their own replication. Poliovirus, a prototypical small positive-strand RNA virus that replicates and assembles in the cytoplasm of the host cell, utilizes membranes derived from the autophagic pathway to aid viral replication and egress from the cell. Recently we made the surprising discovery that GFP-LC3-staining vesicles are physically immobilized during poliovirus infection. Here we discuss our model for the mechanism of vesicle immobilization and the predictions it makes for pathogens that subvert the autophagic pathway to their own ends.
authors.affiliation: Department of Molecular Biology, Princeton University, Princeton, NJ, USA.
authors.forename: Matthew P
authors.initials: MP
authors.lastname: Taylor
authors.forename: William T
authors.initials: WT
authors.lastname: Jackson
mesh_terms: D000818:Animals; D049452:Green Fluorescent Proteins / Q000378:metabolism; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D008954:Models, Biological; D009154:Mutation / Q000235:genetics; D010588:Phagosomes / Q000821:virology*; D017955:Poliovirus / Q000502:physiology*; D014764:Viral Proteins / Q000378:metabolism
chemical_list: D008869:Microtubule-Associated Proteins; D014764:Viral Proteins; D049452:Green Fluorescent Proteins