Evidence map›Paper›PMID 25355889›Full record

ArticleJournal of virology2015

Simian hemorrhagic fever virus cell entry is dependent on CD163 and uses a clathrin-mediated endocytosis-like pathway.

Yíngyún Caì, Elena N Postnikova, John G Bernbaum, Shu Qìng Yú, Steven Mazur, Nicole M Deiuliis, Sheli R Radoshitzky, Matthew G Lackemeyer, Adam McCluskey, Phillip J Robinson and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

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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

19 authors at 5 institutions in 3 countries.

Yíngyún CaìIntegrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland, USA.ORCID http://orcid.org/0000-0002-1101-0920
Elena N PostnikovaIntegrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland, USA.ORCID http://orcid.org/0000-0002-0275-2148
John G BernbaumIntegrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland, USA.ORCID http://orcid.org/0000-0002-1529-8191
Shu Qìng YúIntegrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland, USA.ORCID http://orcid.org/0000-0002-9473-566X
Steven MazurIntegrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland, USA.ORCID http://orcid.org/0000-0002-9349-338X
Nicole M DeiuliisIntegrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland, USA.ORCID http://orcid.org/0000-0002-8923-0288
Sheli R RadoshitzkyUnited States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, Maryland, USA.ORCID http://orcid.org/0000-0001-8976-8056
Matthew G LackemeyerIntegrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland, USA.ORCID http://orcid.org/0000-0002-2174-9630
Adam McCluskeyDepartment of Chemistry, Centre for Chemical Biology, School of Environmental and Life Sciences, University of Newcastle, Callaghan, New South Wales, Australia.
Phillip J RobinsonCell Signaling Unit, Children's Medical Research Institute, The University of Sydney, Sydney, New South Wales, Australia.
Volker HauckeLeibniz Institut für Molekulare Pharmakologie, Berlin, Germany.
Victoria Wahl-JensenIntegrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland, USA.
Adam L BaileyWisconsin National Primate Research Center, Madison, Wisconsin, USA.
Michael LauckWisconsin National Primate Research Center, Madison, Wisconsin, USA.
Thomas C FriedrichWisconsin National Primate Research Center, Madison, Wisconsin, USA.
David H O'ConnorWisconsin National Primate Research Center, Madison, Wisconsin, USA.ORCID http://orcid.org/0000-0003-2139-470X
Tony L GoldbergWisconsin National Primate Research Center, Madison, Wisconsin, USA.
Peter B JahrlingIntegrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland, USA.ORCID http://orcid.org/0000-0002-9775-3724
Jens H KuhnIntegrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland, USA kuhnjens@mail.nih.gov.ORCID http://orcid.org/0000-0002-7800-6045
National Institutes of Health · USLeibniz-Forschungsinstitut für Molekulare Pharmakologie · DEThe University of Sydney · AUUnited States Army Medical Research Institute of Infectious Diseases · USUniversity of Newcastle Australia · AU

Funding

Integrated Research Facility at Fort DetrickZIDAI009006 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI COE, LINDA · 2009 to 2018
$341.7M
WNPRC Supplemental Request for Nonhuman Primate Enclosures to Equip HIV/AIDS-Related Research FacilitiesP51OD011106 · OD · UNIVERSITY OF WISCONSIN-MADISON · PI Dorota A. Grejner-Brzezinska · 2012 to 2026
$150.7M
Pathogenesis and countermeasures of poxviruses, hemorrhagic fever viruses, MERSZIAAI001025 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI JOHNSON, REED · 2009 to 2018
$14.1M
INTEGRATED TRAINING FOR PHYSICIAN-SCIENTISTST32GM008692 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI BURKARD, MARK E · 1998 to 2020
$10.3M
Graduate Training In Cellular And Molecular Pathogenesis Of Human DiseasesT32GM081061 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2010 to 2019
$1.8M
NIAID NIH HHS HHSN272200700016INIGMS NIH HHS T32 GM008692NIGMS NIH HHS T32 GM081061NIH HHS P51 OD011106
6 · The paper itself

Abstract

unlabelledSimian hemorrhagic fever virus (SHFV) causes a severe and almost uniformly fatal viral hemorrhagic fever in Asian macaques but is thought to be nonpathogenic for humans. To date, the SHFV life cycle is almost completely uncharacterized on the molecular level. Here, we describe the first steps of the SHFV life cycle. Our experiments indicate that SHFV enters target cells by low-pH-dependent endocytosis. Dynamin inhibitors, chlorpromazine, methyl-β-cyclodextrin, chloroquine, and concanamycin A dramatically reduced SHFV entry efficiency, whereas the macropinocytosis inhibitors EIPA, blebbistatin, and wortmannin and the caveolin-mediated endocytosis inhibitors nystatin and filipin III had no effect. Furthermore, overexpression and knockout study and electron microscopy results indicate that SHFV entry occurs by a dynamin-dependent clathrin-mediated endocytosis-like pathway. Experiments utilizing latrunculin B, cytochalasin B, and cytochalasin D indicate that SHFV does not hijack the actin polymerization pathway. Treatment of target cells with proteases (proteinase K, papain, α-chymotrypsin, and trypsin) abrogated entry, indicating that the SHFV cell surface receptor is a protein. Phospholipases A2 and D had no effect on SHFV entry. Finally, treatment of cells with antibodies targeting CD163, a cell surface molecule identified as an entry factor for the SHFV-related porcine reproductive and respiratory syndrome virus, diminished SHFV replication, identifying CD163 as an important SHFV entry component. IMPORTANCE: Simian hemorrhagic fever virus (SHFV) causes highly lethal disease in Asian macaques resembling human illness caused by Ebola or Lassa virus. However, little is known about SHFV's ecology and molecular biology and the mechanism by which it causes disease. The results of this study shed light on how SHFV enters its target cells. Using electron microscopy and inhibitors for various cellular pathways, we demonstrate that SHFV invades cells by low-pH-dependent, actin-independent endocytosis, likely with the help of a cellular surface protein.

Indexed as

EndocytosisHost-Pathogen InteractionsVirus InternalizationAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticArterivirusCD163 AntigenCell LineChlorocebus aethiopsReceptors, Cell SurfaceReceptors, VirusAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenReceptors, Cell SurfaceReceptors, Virus

Identifiers

PMID25355889
PMCPMC4301170
OpenAlexW2018229395

What OpenQuestion holds

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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.