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Cited by 818

The DOI matches its Crossref record; 90 of the 90 references it cites were found in a registry or an index.

Subversion of Cellular Autophagosomal Machinery by RNA Viruses

Open access
Jackson, William T, Giddings, Thomas H, Taylor, Matthew P, Mulinyawe, Sara, Rabinovitch, Marlene, Kopito, Ron R, Kirkegaard, Karla·2005·PLoS Biology
DOI 10.1371/journal.pbio.0030156
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Abstract

Infection of human cells with poliovirus induces the proliferation of double-membraned cytoplasmic vesicles whose surfaces are used as the sites of viral RNA replication and whose origin is unknown. Here, we show that several hallmarks of cellular autophagosomes can be identified in poliovirus-induced vesicles, including colocalization of LAMP1 and LC3, the human homolog of Saccharomyces cerevisiae Atg8p, and staining with the fluorophore monodansylcadaverine followed by fixation. Colocalization of LC3 and LAMP1 was observed early in the poliovirus replicative cycle, in cells infected with rhinoviruses 2 and 14, and in cells that express poliovirus proteins 2BC and 3A, known to be sufficient to induce double-membraned vesicles. Stimulation of autophagy increased poliovirus yield, and inhibition of the autophagosomal pathway by 3-methyladenine or by RNA interference against mRNAs that encode two different proteins known to be required for autophagy decreased poliovirus yield. We propose that, for poliovirus and rhinovirus, components of the cellular machinery of autophagosome formation are subverted to promote viral replication. Although autophagy can serve in the innate immune response to microorganisms, our findings are inconsistent with a role for the induced autophagosome-like structures in clearance of poliovirus. Instead, we argue that these double-membraned structures provide membranous supports for viral RNA replication complexes, possibly enabling the nonlytic release of cytoplasmic contents, including progeny virions, from infected cells.

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Citations

Cites

Research works printed but not linked: 6

  1. Irurzun, 1992, Virology, 191, 166, 10.1016/0042-6822(92)90178-R · doi:10.1016/0042-6822(92)90178-r
  2. Aldabe, 1995, Biochem Biophys Res Commun, 206, 64, 10.1006/bbrc.1995.1010 · doi:10.1006/bbrc.1995.1010
  3. Biederbick, 1995, Eur J Cell Biol, 66, 3
  4. Miller, 2003, J Virol, 77, 12193, 10.1128/JVI.77.22.12193-12202.2003 · doi:10.1128/jvi.77.22.12193-12202.2003
  5. Newman, 1973, J Gen Virol, 18, 171, 10.1099/0022-1317-18-2-171 · doi:10.1099/0022-1317-18-2-171
  6. Piirainen, 1998, Microb Pathog, 25, 131, 10.1006/mpat.1998.0221 · doi:10.1006/mpat.1998.0221

Cited by

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Metadata

Authors
Jackson, W. T., Giddings, T. H., Taylor, M. P., Mulinyawe, S., Rabinovitch, M., Kopito, R. R., & Kirkegaard, K.
Venue
PLoS Biology
Publisher
Public Library of Science (PLoS)
Published
2005-04-26
Volume
3
Issue
5
Pages
e156
ISSN
  • 1544-9173 (ISSN-L)
  • 1545-7885
DOI
10.1371/journal.pbio.0030156
OpenAlex
W2079046408
Cited by
818
References
90
FWCI
20.94
Type
journal article
Language
en
Open access
gold
Licence
creativecommons.org/licenses/by/4.0/ (unspecified)

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