Evidence map›Paper›PMID 28742857›Full record

ArticlePloS one2017

DNA-immunisation with dengue virus E protein domains I/II, but not domain III, enhances Zika, West Nile and Yellow Fever virus infection.

Jose L Slon Campos, Monica Poggianella, Sara Marchese, Monica Mossenta, Jyoti Rana, Francesca Arnoldi, Marco Bestagno, Oscar R Burrone

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
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  6. Zika Virus Envelope Protein Domain III Produced inDiagnostics (Basel, Switzerland) · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. CD4Cell reports · 2020
    Article
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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.

Jose L Slon CamposMolecular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Monica PoggianellaMolecular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Sara MarcheseMolecular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Monica MossentaMolecular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Jyoti RanaMolecular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Francesca ArnoldiMolecular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Marco BestagnoMolecular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Oscar R BurroneMolecular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.ORCID http://orcid.org/0000-0003-2682-7332
International Centre for Genetic Engineering and Biotechnology · ITUniversity of Trieste · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dengue virus (DENV), the causative agent of dengue disease, is among the most important mosquito-borne pathogens worldwide. DENV is composed of four closely related serotypes and belongs to the Flaviviridae family alongside other important arthropod-borne viral pathogens such as Zika virus (ZIKV), West Nile virus (WNV) and Yellow Fever virus (YFV). After infection, the antibody response is mostly directed to the viral E glycoprotein which is composed of three structural domains named DI, DII and DIII that share variable degrees of homology among different viruses. Recent evidence supports a close serological interaction between ZIKV and DENV. The possibility of worse clinical outcomes as a consequence of antibody-dependent enhancement of infection (ADE) due to cross-reactive antibodies with poor neutralisation activity is a matter of concern. We tested polyclonal sera from groups of female Balb/C mice vaccinated with DNA constructs expressing DI/DII, DIII or the whole sE from different DENV serotypes and compared their activity in terms of cross-reactivity, neutralisation of virus infection and ADE. Our results indicate that the polyclonal antibody responses against the whole sE protein are highly cross-reactive with strong ADE and poor neutralisation activities due to DI/DII immunodominance. Conversely, anti-DIII polyclonal antibodies are type-specific, with no ADE towards ZIKV, WNV and YFV, and strong neutralisation activity restricted only to DENV.

Indexed as

AnimalsAntibodies, NeutralizingCross ReactionsDengueDengue VirusFemaleImmunizationMiceMice, Inbred BALB CViral Envelope ProteinsWest Nile FeverWest Nile virusYellow FeverYellow fever virusZika VirusZika Virus InfectionAntibodies, NeutralizingE-glycoprotein, Dengue virus type 1E-glycoprotein, Dengue virus type 2E-glycoprotein, Dengue virus type 3glycoprotein E, dengue virus type 4Viral Envelope Proteins

Identifiers

PMID28742857
PMCPMC5526558
OpenAlexW2737790159

What OpenQuestion holds

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Registered trials

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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.