Evidence map›Paper›PMID 26024394›Full record

ReviewCell death and differentiation2015

Molecular mechanisms of Ebola virus pathogenesis: focus on cell death.

L Falasca, C Agrati, N Petrosillo, A Di Caro, M R Capobianchi, G Ippolito, M Piacentini

Open access · hybridAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 3 pooled it
9.5field-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

95 citing papers in PubMed, 3 syntheses or guidelines pooled it, 163 citations in OpenAlex.

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  14. Direct Intercellular Transport Mode of Filovirus Nucleocapsids.International journal of molecular sciences · 2025
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35 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

7 authors at 2 institutions in 1 country.

L FalascaNational Institute for Infectious Diseases, Lazzaro Spallanzani, Rome, Italy.
C AgratiNational Institute for Infectious Diseases, Lazzaro Spallanzani, Rome, Italy.
N PetrosilloNational Institute for Infectious Diseases, Lazzaro Spallanzani, Rome, Italy.
A Di CaroNational Institute for Infectious Diseases, Lazzaro Spallanzani, Rome, Italy.
M R CapobianchiNational Institute for Infectious Diseases, Lazzaro Spallanzani, Rome, Italy.
G IppolitoNational Institute for Infectious Diseases, Lazzaro Spallanzani, Rome, Italy.
M Piacentini1] National Institute for Infectious Diseases, Lazzaro Spallanzani, Rome, Italy [2] Department of Biology, University of Rome Tor Vergata, Rome, Italy.
Istituto Nazionale per le Malattie Infettive Lazzaro Spallanzani · ITUniversity of Rome Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ebola virus (EBOV) belongs to the Filoviridae family and is responsible for a severe disease characterized by the sudden onset of fever and malaise accompanied by other non-specific signs and symptoms; in 30-50% of cases hemorrhagic symptoms are present. Multiorgan dysfunction occurs in severe forms with a mortality up to 90%. The EBOV first attacks macrophages and dendritic immune cells. The innate immune reaction is characterized by a cytokine storm, with secretion of numerous pro-inflammatory cytokines, which induces a huge number of contradictory signals and hurts the immune cells, as well as other tissues. Other highly pathogenic viruses also trigger cytokine storms, but Filoviruses are thought to be particularly lethal because they affect a wide array of tissues. In addition to the immune system, EBOV attacks the spleen and kidneys, where it kills cells that help the body to regulate its fluid and chemical balance and that make proteins that help the blood to clot. In addition, EBOV causes liver, lungs and kidneys to shut down their functions and the blood vessels to leak fluid into surrounding tissues. In this review, we analyze the molecular mechanisms at the basis of Ebola pathogenesis with a particular focus on the cell death pathways induced by the virus. We also discuss how the treatment of the infection can benefit from the recent experience of blocking/modulating cell death in human degenerative diseases.

Indexed as

Cell DeathDendritic CellsEbolavirusHemorrhagic Fever, EbolaHumansMacrophages

Identifiers

PMID26024394
PMCPMC4495366
OpenAlexW1526693451

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.