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Journal of Virology, July 2009, p. 6599-6609, Vol. 83, No. 13
0022-538X/09/$08.00+0     doi:10.1128/JVI.01819-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Role of Microtubules in Extracellular Release of Poliovirus{triangledown} ,{dagger}

Matthew P. Taylor,1,{ddagger} Trever B. Burgon,1 Karla Kirkegaard,1* and William T. Jackson2

Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California,1 Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin2

Received 29 August 2008/ Accepted 3 April 2009

Cellular autophagy, a process that directs cytosolic contents to the endosomal and lysosomal pathways via the formation of double-membraned vesicles, is a crucial aspect of innate immunity to many intracellular pathogens. However, evidence is accumulating that certain RNA viruses, such as poliovirus, subvert this pathway to facilitate viral growth. The autophagosome-like membranes induced during infection with wild-type poliovirus were found to be, unlike cellular autophagosomes, relatively immobile. Their mobility increased upon nocodazole treatment, arguing that vesicular tethering is microtubule dependent. In cells infected with a mutant virus that is defective in its interaction with the host cytoskeleton and secretory pathway, vesicle movement increased, indicating reduced tethering. In all cases, the release of tethering correlated with increased amounts of extracellular virus, which is consistent with the hypothesis that small amounts of cytosol and virus entrapped by double-membraned structures could be released via fusion with the plasma membrane. We propose that this extracellular delivery of cytoplasmic contents be termed autophagosome-mediated exit without lysis (AWOL). This pathway could explain the observed exit, in the apparent absence of cellular lysis, of other cytoplasmic macromolecular complexes, including infectious agents and complexes of aggregated proteins.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Fairchild Science Building D309A, Stanford University School of Medicine, Stanford, CA 94305-5402. Phone: (650) 498-7075. Fax: (650) 498-7147. E-mail: karlak{at}stanford.edu

{triangledown} Published ahead of print on 15 April 2009.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

{ddagger} Present address: Department of Molecular Biology, Princeton University, Princeton, NJ 08544.

Journal of Virology, July 2009, p. 6599-6609, Vol. 83, No. 13
0022-538X/09/$08.00+0     doi:10.1128/JVI.01819-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



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