Evidence map›Paper›PMID 23345511›Full record

ArticleJournal of virology2013

Ebola virus exploits a monocyte differentiation program to promote its entry.

Osvaldo Martinez, Joshua C Johnson, Anna Honko, Benjamin Yen, Reed S Shabman, Lisa E Hensley, Gene G Olinger, Christopher F Basler

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

42 citing papers in PubMed, 70 citations in OpenAlex.

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  6. Extracellular vesicle storm during the course of Ebola virus infection in primates.Frontiers in cellular and infection microbiology · 2023
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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

8 authors at 2 institutions in 1 country.

Osvaldo MartinezIcahn School of Medicine at Mount Sinai, New York, New York, USA.
Joshua C Johnson
Anna Honko
Benjamin Yen
Reed S Shabman
Lisa E Hensley
Gene G Olinger
Christopher F Basler
Icahn School of Medicine at Mount Sinai · USUnited States Army Medical Research Institute of Infectious Diseases · US

Funding

Viral Pathogenesis and TherapeuticsU54AI057158 · NIAID · WADSWORTH CENTER · PI LIPKIN, W. IAN · 2003 to 2014
$100.8M
Ebola VP35 Interferon-Antagonist: Mechanism and SignifR01AI059536 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BASLER, CHRISTOPHER F · 2005 to 2015
$4.2M
p38 MAP kinase inhibitors as therapeutics targeting ebolavirus entryR21AI097568 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BASLER, CHRISTOPHER F · 2012 to 2013
$457k
Ebola virus VP24 alters hnRNP C nuclear import: implications for replicationF32AI084453 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SHABMAN, REED SOLOMON · 2009 to 2010
$98k
NIAID NIH HHS 5F32AI084453-02NIAID NIH HHS AI057158NIAID NIH HHS F32 AI084453NIAID NIH HHS R01 AI059536NIAID NIH HHS R01AI059536NIAID NIH HHS R21 AI097568NIAID NIH HHS R21AI097568NIAID NIH HHS U54 AI057158
6 · The paper itself

Abstract

Antigen-presenting cells (APCs) are critical targets of Ebola virus (EBOV) infection in vivo. However, the susceptibility of monocytes to infection is controversial. Studies indicate productive monocyte infection, and yet monocytes are also reported to be resistant to EBOV GP-mediated entry. In contrast, monocyte-derived macrophages and dendritic cells are permissive for both EBOV entry and replication. Here, freshly isolated monocytes are demonstrated to indeed be refractory to EBOV entry. However, EBOV binds monocytes, and delayed entry occurs during monocyte differentiation. Cultured monocytes spontaneously downregulate the expression of viral entry restriction factors such as interferon-inducible transmembrane proteins, while upregulating the expression of critical EBOV entry factors cathepsin B and NPC1. Moreover, these processes are accelerated by EBOV infection. Finally, ectopic expression of NPC1 is sufficient to rescue entry into an undifferentiated, normally nonpermissive monocytic cell line. These results define the molecular basis for infection of APCs and suggest means to limit APC infection.

Indexed as

Virus AttachmentVirus InternalizationCarrier ProteinsCathepsin BCell DifferentiationDendritic CellsDNA PrimersEbolavirusFlow CytometryHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsMacrophagesMembrane GlycoproteinsMonocytesNiemann-Pick C1 ProteinCarrier ProteinsCathepsin BDNA PrimersIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsNiemann-Pick C1 ProteinNPC1 protein, human

Identifiers

PMID23345511
PMCPMC3624207
OpenAlexW2129860769

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.