Evidence map›Paper›PMID 26698106›Full record

ArticleeLife2015

Filovirus receptor NPC1 contributes to species-specific patterns of ebolavirus susceptibility in bats.

Melinda Ng, Esther Ndungo, Maria E Kaczmarek, Andrew S Herbert, Tabea Binger, Ana I Kuehne, Rohit K Jangra, John A Hawkins, Robert J Gifford, Rohan Biswas and 11 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

86 citing papers in PubMed, 136 citations in OpenAlex.

  1. Article
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  6. Review
  7. The Journal of general virology · 2025
    Article
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  13. Ecological monographs · 2025
    Article
  14. Article
  15. Review
  16. Article
  17. Molecular determinants of cross-species transmission in emerging viral infections.Microbiology and molecular biology reviews : MMBR · 2024
    Review
  18. Article
  19. Article
  20. Article

26 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

21 authors at 9 institutions in 5 countries.

Melinda NgDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, United States.
Esther NdungoDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, United States.
Maria E KaczmarekDepartment of Integrative Biology, University of Texas at Austin, Austin, United States.
Andrew S HerbertUnited States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, United States.
Tabea BingerInstitute of Virology, University of Bonn Medical Center, Bonn, Germany.
Ana I KuehneUnited States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, United States.
Rohit K JangraDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, United States.
John A HawkinsInstitute for Computational Engineering and Sciences, University of Texas at Austin, Austin, United States.
Robert J GiffordUniversity of Glasgow MRC Virology Unit, Glasgow, United Kingdom.
Rohan BiswasDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, United States.
Ann DemoginesDepartment of Molecular Biosciences, University of Texas at Austin, Austin, United States.
Rebekah M JamesUnited States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, United States.
Meng YuProgram in Emerging Infectious Diseases, Duke-NUS Graduate Medical School, , Singapore.
Thijn R BrummelkampNetherlands Cancer Institute, Plesmanlaan, The Netherlands.
Christian DrostenInstitute of Virology, University of Bonn Medical Center, Bonn, Germany.
Lin-Fa WangProgram in Emerging Infectious Diseases, Duke-NUS Graduate Medical School, , Singapore.
Jens H KuhnIntegrated Research Facility at Fort Detrick, National Institute for Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, United States.ORCID http://orcid.org/0000-0002-7800-6045
Marcel A MüllerInstitute of Virology, University of Bonn Medical Center, Bonn, Germany.
John M DyeUnited States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, United States.
Sara L SawyerDepartment of Molecular Biosciences, University of Texas at Austin, Austin, United States.
Kartik ChandranDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, United States.ORCID http://orcid.org/0000-0003-0232-7077
Albert Einstein College of Medicine · USUnited States Army Medical Research Institute of Infectious Diseases · USThe University of Texas at Austin · USUniversity of Bonn · DEDuke-NUS Medical School · SGMRC University of Glasgow Centre for Virus Research · GBNational Institutes of Health · USThe Netherlands Cancer Institute · NLUniversity of Colorado Boulder · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
Mechanism of receptor-mediated entry and infection by filovirusesR01AI101436 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CHANDRAN, KARTIK · 2012 to 2016
$4.0M
Mechanisms of Ebolavirus and Marburgvirus Entry into CellsR01AI088027 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CHANDRAN, KARTIK · 2010 to 2014
$2.0M
Rapid evolution of genes critical for genome integrityR01GM093086 · NIGMS · UNIVERSITY OF TEXAS AT AUSTIN · PI SAWYER, SARA · 2010 to 2016
$1.9M
NIAID NIH HHS AI101436NIAID NIH HHS R01 AI088027NIAID NIH HHS R01 AI101436NIGMS NIH HHS GM093086NIGMS NIH HHS R01 GM093086NIGMS NIH HHS T32 GM007288
6 · The paper itself

Abstract

Biological factors that influence the host range and spillover of Ebola virus (EBOV) and other filoviruses remain enigmatic. While filoviruses infect diverse mammalian cell lines, we report that cells from African straw-colored fruit bats (Eidolon helvum) are refractory to EBOV infection. This could be explained by a single amino acid change in the filovirus receptor, NPC1, which greatly reduces the affinity of EBOV-NPC1 interaction. We found signatures of positive selection in bat NPC1 concentrated at the virus-receptor interface, with the strongest signal at the same residue that controls EBOV infection in Eidolon helvum cells. Our work identifies NPC1 as a genetic determinant of filovirus susceptibility in bats, and suggests that some NPC1 variations reflect host adaptations to reduce filovirus replication and virulence. A single viral mutation afforded escape from receptor control, revealing a pathway for compensatory viral evolution and a potential avenue for expansion of filovirus host range in nature.

Indexed as

Host SpecificityVirus AttachmentAnimalsCell LineChiropteraFiloviridaeMembrane GlycoproteinsReceptors, VirusMembrane GlycoproteinsReceptors, VirusbatsEbola virusevolutionary biologyFilovirusgenomicshost rangeinfectious diseasemicrobiologyNiemann-Pick C1NPC1Positive selectionviral receptorvirusesVirus-host co-evolution

Identifiers

PMID26698106
PMCPMC4709267
OpenAlexW2206668730

What OpenQuestion holds

Textmetadata
LicenceCC0
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.