Evidence map›Paper›PMID 21738474›Full record

ArticlePLoS pathogens2011

The SV40 late protein VP4 is a viroporin that forms pores to disrupt membranes for viral release.

Smita Raghava, Kristina M Giorda, Fabian B Romano, Alejandro P Heuck, Daniel N Hebert

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
6.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
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  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Human polyomaviruses and cancer: an overview.Clinics (Sao Paulo, Brazil) · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Cell Walls and the Convergent Evolution of the Viral Envelope.Microbiology and molecular biology reviews : MMBR · 2015
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Smita RaghavaDepartment of Biochemistry and Molecular Biology, Program in Molecular and Cellular Biology, University of Massachusetts, Amherst, Massachusetts, United States of America.
Kristina M Giorda
Fabian B Romano
Alejandro P Heuck
Daniel N Hebert
University of Massachusetts Amherst · US

Funding

CHEMISTRY-BIOLOGY INTERFACE PREDOCTORAL TRAINING GRANTST32GM008515 · NIGMS · UNIVERSITY OF MASSACHUSETTS AMHERST · PI THOMPSON, LYNMARIE K. · 1995 to 2020
$4.3M
Simian Virus 40 (SV40) uncoating and penetrationR21AI078142 · NIAID · UNIVERSITY OF MASSACHUSETTS AMHERST · PI HEBERT, DANIEL N. · 2008 to 2009
$422k
NIAID NIH HHS AI078142NIAID NIH HHS R21 AI078142NIGMS NIH HHS T32GM00815NIGMS NIH HHS T32 GM008515
6 · The paper itself

Abstract

Nonenveloped viruses are generally released by the timely lysis of the host cell by a poorly understood process. For the nonenveloped virus SV40, virions assemble in the nucleus and then must be released from the host cell without being encapsulated by cellular membranes. This process appears to involve the well-controlled insertion of viral proteins into host cellular membranes rendering them permeable to large molecules. VP4 is a newly identified SV40 gene product that is expressed at late times during the viral life cycle that corresponds to the time of cell lysis. To investigate the role of this late expressed protein in viral release, water-soluble VP4 was expressed and purified as a GST fusion protein from bacteria. Purified VP4 was found to efficiently bind biological membranes and support their disruption. VP4 perforated membranes by directly interacting with the membrane bilayer as demonstrated by flotation assays and the release of fluorescent markers encapsulated into large unilamellar vesicles or liposomes. The central hydrophobic domain of VP4 was essential for membrane binding and disruption. VP4 displayed a preference for membranes comprised of lipids that replicated the composition of the plasma membranes over that of nuclear membranes. Phosphatidylethanolamine, a lipid found at high levels in bacterial membranes, was inhibitory against the membrane perforation activity of VP4. The disruption of membranes by VP4 involved the formation of pores of ∼3 nm inner diameter in mammalian cells including permissive SV40 host cells. Altogether, these results support a central role of VP4 acting as a viroporin in the perforation of cellular membranes to trigger SV40 viral release.

Indexed as

Cell MembraneFluorescent Antibody TechniqueGlutathione TransferaseLiposomesPhosphatidylethanolaminesPorinsPorosityRecombinant Fusion ProteinsSequence DeletionSimian virus 40Viral Structural ProteinsVirus ReleaseGlutathione TransferaseLiposomesphosphatidylethanolaminePhosphatidylethanolaminesPorinsRecombinant Fusion ProteinsViral Structural Proteins

Identifiers

PMID21738474
PMCPMC3128117
OpenAlexW2009328514

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.