Evidence map›Paper›PMID 15657120›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Pathogenic hantaviruses bind plexin-semaphorin-integrin domains present at the apex of inactive, bent alphavbeta3 integrin conformers.

Tracy Raymond, Elena Gorbunova, Irina N Gavrilovskaya, Erich R Mackow

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

67 citing papers in PubMed, 102 citations in OpenAlex.

  1. Review
  2. Article
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  4. Therapeutic potential for P2YPurinergic signalling · 2023
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  12. Article
  13. Endothelial Cells in Emerging Viral Infections.Frontiers in cardiovascular medicine · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Hantavirus entry: Perspectives and recent advances.Advances in virus research · 2019
    Article
  19. Article
  20. Article

7 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Tracy RaymondDepartment of Medicine and Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, NY 11794, USA.
Elena Gorbunova
Irina N Gavrilovskaya
Erich R Mackow
Northport VA Medical Center · USStony Brook University · US

Funding

Virulence Mechanism of Y. pestis and tularensisP01AI055621 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI BENACH, JORGE L. · 2004 to 2010
$20.7M
HANTAVIRUS CELL INTERACTIONSR01AI047873 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI MACKOW, ERICH R. · 2000 to 2003
$1.1M
Determinants of Pathogenic Hantavirus AttachmentR21AI080984 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI MACKOW, ERICH R · 2009 to 2010
$430k
NIAID NIH HHS P01 AI055621NIAID NIH HHS R01 AI047873NIAID NIH HHS R01AI47873NIAID NIH HHS R21 AI080984
6 · The paper itself

Abstract

The alphavbeta3 integrins are linked to human bleeding disorders, and pathogenic hantaviruses regulate the function of alphavbeta3 integrins and cause acute vascular diseases. alphavbeta3 integrins are present in either extended (active) or dramatically bent (inactive) structures, and interconversion of alphavbeta3 conformers dynamically regulates integrin functions. Here, we show that hantaviruses bind human alphavbeta3 integrins and that binding maps to the plexin-semaphorin-integrin (PSI) domain present at the apex of inactive, bent, alphavbeta3-integrin structures. Pathogenic hantaviruses [New York-1 virus (NY-1V) and Hantaan virus (HTNV)] bind immobilized beta3 polypeptides containing the PSI domain, and human (but not murine) beta3 polypeptides inhibit hantavirus infectivity. Substitution of human beta3 residues 1-39 for murine beta3 residues directed pathogenic hantavirus infection of nonpermissive CHO cells expressing chimeric alphavbeta3 receptors. Mutation of murine beta3 Asn-39 to Asp-39 present in human beta3 homologues (N39D) permitted hantavirus infection of cells and specified PSI domain residue interactions with pathogenic hantaviruses. In addition, cell-surface expression of alphavbeta3 locked in an inactive bent conformation conferred hantavirus infectivity of CHO cells. Our findings indicate that hantaviruses bind to a unique domain exposed on inactive integrins and, together with prior findings, suggest that this interaction restricts alphavbeta3 functions that regulate vascular permeability. Our findings suggest mechanisms for viruses to direct hemorrhagic or vascular diseases and provide a distinct target for modulating alphavbeta3-integrin functions.

Indexed as

Amino Acid SequenceAnimalsCapillary PermeabilityCell Adhesion MoleculesCHO CellsCricetinaeDimerizationHumansIntegrin alphaVbeta3MiceMolecular Sequence DataNerve Tissue ProteinsOligopeptidesOrthohantavirusProtein ConformationSemaphorinsarginyl-glycyl-aspartic acidCell Adhesion MoleculesIntegrin alphaVbeta3Nerve Tissue ProteinsOligopeptidesplexinSemaphorins

Identifiers

PMID15657120
PMCPMC545842
OpenAlexW2070593205

What OpenQuestion holds

Textmetadata
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.