Evidence map›Paper›PMID 28555386›Full record

ReviewSeminars in immunopathology2017

Molecular pathogenesis of viral hemorrhagic fever.

Christopher F Basler

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Host Glycan-Lectin Interplay in SARS-CoV-2 Infection.International journal of molecular sciences · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Lassa Fever: Critical Review and Prospects for Control.Tropical medicine and infectious disease · 2024
    Review
  11. Recent Advances in Therapeutic Approaches Against Ebola Virus Infection.Recent advances in anti-infective drug discovery · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Crimean-Congo haemorrhagic fever virus.Nature reviews. Microbiology · 2023
    Review
  17. Article
  18. Review
  19. Cheminformatics-Based Study Identifies Potential Ebola VP40 Inhibitors.International journal of molecular sciences · 2023
    Article
  20. Article
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

1 author at 1 institution in 1 country.

Christopher F BaslerCenter for Microbial Pathogenesis, Georgia Research Alliance Eminent Scholar in Microbial Pathogenesis, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, 30303, USA. cbasler@gsu.edu.ORCID 0000-0003-4195-425X
Georgia State University · US

Funding

Molecular mechanisms of immune dysregulation by filoviral interferon U19AI109945 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BASLER, CHRISTOPHER F · 2014 to 2018
$9.5M
NIAID NIH HHS U19 AI109945
6 · The paper itself

Abstract

The clinical syndrome referred to as viral hemorrhagic fever (VHF) can be caused by several different families of RNA viruses, including select members of the arenaviruses, bunyaviruses, filoviruses, and flaviviruses. VHF is characterized by malaise, fever, vascular permeability, decreased plasma volume, coagulation abnormalities, and varying degrees of hemorrhage. Study of the filovirus Ebola virus has demonstrated a critical role for suppression of innate antiviral defenses in viral pathogenesis. Additionally, antigen-presenting cells are targets of productive infection and immune dysregulation. Among these cell populations, monocytes and macrophages are proposed to produce damaging inflammatory cytokines, while infected dendritic cells fail to undergo proper maturation, potentially impairing adaptive immunity. Uncontrolled virus replication and accompanying inflammatory responses are thought to promote vascular leakage and coagulopathy. However, the specific molecular pathways that underlie these features of VHF remain poorly understood. The arenavirus Lassa virus and the flavivirus yellow fever virus exhibit similar molecular pathogenesis suggesting common underlying mechanisms. Because non-human primate models that closely mimic VHF are available for Ebola, Lassa, and yellow fever viruses, we propose that comparative molecular studies using these models will yield new insights into the molecular underpinnings of VHF and suggest new therapeutic approaches.

Indexed as

Adaptive ImmunityAnimalsBiomarkersBlood CoagulationCapillary PermeabilityCytokinesDisease SusceptibilityHemorrhagic Fevers, ViralHost-Pathogen InteractionsHumansImmunity, InnateInflammation MediatorsBiomarkersCytokinesInflammation MediatorsEbola virusHemorrhagic feverLassa virusyellow fever virus

Identifiers

PMID28555386
PMCPMC6436832
OpenAlexW2619092125

What OpenQuestion holds

Textmetadata
LicenceTDM
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.