Evidence map›Paper›PMID 28437586›Full record

ReviewImmunology2017

Pathogenesis of vascular leak in dengue virus infection.

Gathsaurie Neelika Malavige, Graham S Ogg

Open access · greenAbstract readReview
In one paragraph

Review in Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 3 pooled it
16.1field-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

158 citing papers in PubMed, 3 syntheses or guidelines pooled it, 263 citations in OpenAlex.

  1. Pooled it
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  13. Discovery of 10-Shogaol fromJournal of agricultural and food chemistry · 2026
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  20. Characterising secondary dengue infections in Saudi Arabia using combined IgG and PCR testing.Transactions of the Royal Society of Tropical Medicine and Hygiene · 2026
    Article

98 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

2 authors at 2 institutions in 2 countries.

Gathsaurie Neelika MalavigeCentre for Dengue Research, University of Sri Jayewardenepura, Nugegoda, Sri Lanka.ORCID 0000-0001-9201-0449
Graham S OggMRC Human Immunology Unit, Radcliffe Department of Medicine, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
University of Oxford · GBUniversity of Sri Jayewardenepura · LK

Funding

Department of HealthMedical Research Council MC_U137881017Medical Research Council MC_UU_12010/5
6 · The paper itself

Abstract

Endothelial dysfunction leading to vascular leak is the hallmark of severe dengue. Vascular leak typically becomes clinically evident 3-6 days after the onset of illness, which is known as the critical phase. This critical phase follows the period of peak viraemia, and lasts for 24-48 hr and usually shows rapid and complete reversal, suggesting that it is likely to occur as a result of inflammatory mediators, rather than infection of the endothelium. Cytokines such as tumour necrosis factor-α, which are known to be elevated in the critical phase of dengue, are likely to be contributing factors. Dengue NS1, a soluble viral protein, has also been shown to disrupt the endothelial glycocalyx and thus contribute to vascular leak, although there appears to be a discordance between the timing of NS1 antigenaemia and occurrence of vascular leak. In addition, many inflammatory lipid mediators are elevated in acute dengue viral infection such as platelet activating factor (PAF) and leukotrienes. Furthermore, many other inflammatory mediators such as vascular endothelial growth factor and angiopoietin-2 have been shown to be elevated in patients with dengue haemorrhagic fever, exerting their action in part by inducing the activity of phospholipases, which have diverse inflammatory effects including generation of PAF. Platelets have also been shown to significantly contribute to endothelial dysfunction by production of interleukin-1β through activation of the NLRP3 inflammasome and also by inducing production of inflammatory cytokines by monocytes. Drugs that block down-stream immunological mediator pathways such as PAF may also be beneficial in the treatment of severe disease.

Indexed as

Capillary PermeabilityAngiopoietinsAnimalsBlood PlateletsCytokinesDengueDengue VirusEndothelium, VascularHumansInflammation MediatorsLeukotrienesMast CellsPlatelet Activating FactorSignal TransductionViral Nonstructural ProteinsAngiopoietinsCytokinesInflammation MediatorsLeukotrienesPlatelet Activating FactorViral Nonstructural Proteinsdenguelipid mediatorsNS1 antigenplatelet activating factorvascular leak

Identifiers

PMID28437586
PMCPMC5461104
OpenAlexW2607859602

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.