Evidence map›Paper›PMID 30212537›Full record

ArticlePLoS pathogens2018

CD4+T cells mediate protection against Zika associated severe disease in a mouse model of infection.

Mariah Hassert, Kyle J Wolf, Katherine E Schwetye, Richard J DiPaolo, James D Brien, Amelia K Pinto

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
12.4field-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

66 citing papers in PubMed, 104 citations in OpenAlex.

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  17. Bystander activated CD8Nature communications · 2024
    Article
  18. Characterization of CD8Journal of virology · 2024
    Article
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  20. Article

6 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

6 authors at 1 institution in 1 country.

Mariah HassertDepartment of Molecular Microbiology and Immunology, Saint Louis University, St Louis, Missouri, United States of America.ORCID 0000-0002-2141-3344
Kyle J WolfDepartment of Molecular Microbiology and Immunology, Saint Louis University, St Louis, Missouri, United States of America.ORCID 0000-0003-4874-2911
Katherine E SchwetyeDepartment of Pathology, Saint Louis University, St. Louis, Missouri, United States of America.ORCID 0000-0002-0885-2764
Richard J DiPaoloDepartment of Molecular Microbiology and Immunology, Saint Louis University, St Louis, Missouri, United States of America.
James D BrienDepartment of Molecular Microbiology and Immunology, Saint Louis University, St Louis, Missouri, United States of America.ORCID 0000-0002-1670-8041
Amelia K PintoDepartment of Molecular Microbiology and Immunology, Saint Louis University, St Louis, Missouri, United States of America.ORCID 0000-0002-7147-3978
Saint Louis University · US

Funding

IMMUNE CONTROL OF WEST NILE VIRUS QUASISPECIES DYNAMICSK22AI104794 · NIAID · SAINT LOUIS UNIVERSITY · PI BRIEN, JAMES D · 2016 to 2017
$269k
NIAID NIH HHS K22 AI104794
6 · The paper itself

Abstract

Zika virus (ZIKV) has gained worldwide attention since it emerged, and a global effort is underway to understand the correlates of protection and develop diagnostics to identify rates of infection. As new therapeutics and vaccine approaches are evaluated in clinical trials, additional effort is focused on identifying the adaptive immune correlates of protection against ZIKV disease. To aid in this endeavor we have begun to dissect the role of CD4+T cells in the protection against neuroinvasive ZIKV disease. We have identified an important role for CD4+T cells in protection, demonstrating that in the absence of CD4+T cells mice have more severe neurological sequela and significant increases in viral titers in the central nervous system (CNS). The transfer of CD4+T cells from ZIKV immune mice protect type I interferon receptor deficient animals from a lethal challenge; showing that the CD4+T cell response is necessary and sufficient for control of ZIKV disease. Using a peptide library spanning the complete ZIKV polyprotein, we identified both ZIKV-encoded CD4+T cell epitopes that initiate immune responses, and ZIKV specific CD4+T cell receptors that recognize these epitopes. Within the ZIKV antigen-specific TCRβ repertoire, we uncovered a high degree of diversity both in response to a single epitope and among different mice responding to a CD4+T cell epitope. Overall this study identifies a novel role for polyfunctional and polyclonal CD4+T cells in providing protection against ZIKV infection and highlights the need for vaccines to develop robust CD4+T cell responses to prevent ZIKV neuroinvasion and limit replication within the CNS.

Indexed as

Adoptive TransferAmino Acid SequenceAnimalsAntigens, ViralCD4-Positive T-LymphocytesCentral Nervous SystemDisease Models, AnimalEpitopes, T-LymphocyteGenes, T-Cell Receptor betaHumansImmunity, CellularLiverLymphocyte DepletionMiceMice, Inbred C57BLMice, KnockoutAntigens, ViralEpitopes, T-LymphocyteIfnar1 protein, mouseReceptor, Interferon alpha-betaViral Vaccines

Identifiers

PMID30212537
PMCPMC6136803
OpenAlexW2889817565

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.