Evidence map›Paper›PMID 35588060›Full record

ArticleJCI insight2022

Cross-reactive antibodies facilitate innate sensing of dengue and Zika viruses.

Laura K Aisenberg, Kimberly E Rousseau, Katherine Cascino, Guido Massaccesi, William H Aisenberg, Wensheng Luo, Kar Muthumani, David B Weiner, Stephen S Whitehead, Michael A Chattergoon and 2 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Mechanisms of Zika astrocyte infection and neuronal toxicity.NeuroImmune pharmacology and therapeutics · 2023
    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

12 authors at 3 institutions in 1 country.

Laura K AisenbergDepartment of Medicine, Division of Infectious Disease, and.
Kimberly E RousseauDepartment of Medicine, Division of Infectious Disease, and.
Katherine CascinoDepartment of Medicine, Division of Infectious Disease, and.
Guido MassaccesiDepartment of Medicine, Division of Infectious Disease, and.
William H AisenbergDepartment of Medicine, Division of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Wensheng LuoCenter for Immunization Research, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA.
Kar MuthumaniThe Wistar Institute, Vaccine & Immunotherapy Center, Philadelphia, Pennsylvania, USA.
David B WeinerThe Wistar Institute, Vaccine & Immunotherapy Center, Philadelphia, Pennsylvania, USA.
Stephen S WhiteheadNational Institute of Allergy and Infectious Diseases, NIH, Laboratory of Viral Diseases, Bethesda, Maryland, USA.
Michael A ChattergoonDepartment of Medicine, Division of Infectious Disease, and.
Anna P DurbinCenter for Immunization Research, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA.
Andrea L CoxDepartment of Medicine, Division of Infectious Disease, and.
Johns Hopkins University · USThe Wistar Institute · USNational Institute of Allergy and Infectious Diseases · US

Funding

Clinical Trials of Biodefense Vaccines (Dengue, West Nile Virus, TBEV)ZIAAI000987 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI WHITEHEAD, STEPHEN · 2009 to 2025
$37.9M
The development and pre-clinical assessment of novel HCV vaccines to generate T and B cell immunityU19AI159822 · NIAID · JOHNS HOPKINS UNIVERSITY · PI COX, ANDREA L · 2021 to 2025
$14.4M
Antibody-Mediated Suppression of Antiviral Inflammasome ActivationR01AI108403 · NIAID · JOHNS HOPKINS UNIVERSITY · PI COX, ANDREA L · 2013 to 2017
$2.2M
Recognition of HIV by the Inflammasome Signaling ComplexK08AI102696 · NIAID · JOHNS HOPKINS UNIVERSITY · PI CHATTERGOON, MICHAEL ANAND · 2013 to 2017
$937k
NIAID NIH HHS K08 AI102696NIAID NIH HHS R01 AI108403NIAID NIH HHS U19 AI159822
6 · The paper itself

Abstract

The Aedes aegypti mosquito transmits both dengue virus (DENV) and Zika virus (ZIKV) . Individuals in endemic areas are at risk for infection with both viruses, as well as for repeated DENV infection. In the presence of anti-DENV antibodies, outcomes of secondary DENV infection range from mild to life threatening. Furthermore, the role of cross-reactive antibodies on the course of ZIKV infection remains unclear. We assessed the ability of cross-reactive DENV mAbs or polyclonal immunoglobulin isolated after DENV vaccination to upregulate type I IFN production by plasmacytoid DCs (pDCs) in response to both heterotypic DENV- and ZIKV-infected cells. We found a range in the ability of antibodies to increase pDC IFN production and a positive correlation between IFN production and the ability of an antibody to bind to the infected cell surface. Engagement of Fc receptors on the pDC and engagement of epitope on the infected cell by the Fab portion of the same antibody molecule was required to mediate increased IFN production by providing specificity to and promoting pDC sensing of DENV or ZIKV. This represents a mechanism independent of neutralization by which preexisting cross-reactive DENV antibodies could protect a subset of individuals from severe outcomes during secondary heterotypic DENV or ZIKV infection.

Indexed as

DengueDengue VirusZika VirusZika Virus InfectionAnimalsCross ReactionsHumansAdaptive immunityImmunologyInfectious diseaseInnate immunity

Identifiers

PMID35588060
PMCPMC9309050
OpenAlexW4280593626

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.