Evidence map›Paper›PMID 29331320›Full record

ArticleAntiviral research2018

Zika, dengue and yellow fever viruses induce differential anti-viral immune responses in human monocytic and first trimester trophoblast cells.

Huanle Luo, Evandro R Winkelmann, Ildefonso Fernandez-Salas, Li Li, Sandra V Mayer, Rogelio Danis-Lozano, Rosa Ma Sanchez-Casas, Nikos Vasilakis, Robert Tesh, Alan D Barrett and 2 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Antiviral research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
7.1field-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

36 citing papers in PubMed, 52 citations in OpenAlex.

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  5. Maternal Immune Activation: Implications for Congenital Heart Defects.Clinical reviews in allergy & immunology · 2025
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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

12 authors at 3 institutions in 2 countries.

Huanle LuoDepartment of Microbiology & Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Evandro R WinkelmannDepartment of Microbiology & Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Ildefonso Fernandez-SalasCentro Regional de Salud Pública, Instituto Nacional de Salud Pública, Tapachula, Mexico.
Li LiDepartment of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Sandra V MayerDepartment of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Rogelio Danis-LozanoCentro Regional de Salud Pública, Instituto Nacional de Salud Pública, Tapachula, Mexico.
Rosa Ma Sanchez-CasasFMVZ/CIDICS, Universidad Autonoma de Nuevo Leon, Monterrey, NL, Mexico.
Nikos VasilakisDepartment of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA; Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, TX 77555, USA; Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, USA.
Robert TeshDepartment of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA; Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, TX 77555, USA; Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, USA.
Alan D BarrettDepartment of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA; Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, TX 77555, USA; Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, USA.
Scott C WeaverDepartment of Microbiology & Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA; Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA; Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, TX 77555, USA; Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, USA.
Tian WangDepartment of Microbiology & Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA; Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA; Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, TX 77555, USA; Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, USA. Electronic address: ti1wang@utmb.edu.
The University of Texas Medical Branch at Galveston · USInstituto Nacional de Salud Pública · MXUniversidad Autónoma de Nuevo León · MX

Funding

World Reference Center for Emerging Viruses and Arboviruses (WRCEVA)R24AI120942 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI WEAVER, SCOTT C · 2016 to 2024
$8.5M
Rational Development of Candidate Attenuated Flavivirus VaccinesR01AI099123 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI WANG, TIAN · 2013 to 2016
$1.8M
NIAID NIH HHS R01 AI099123NIAID NIH HHS R24 AI120942
6 · The paper itself

Abstract

Zika virus (ZIKV) is a mosquito-borne flavivirus associated with severe neonatal birth defects, but the causative mechanism is incompletely understood. ZIKV shares sequence homology and early clinical manifestations with yellow fever virus (YFV) and dengue virus (DENV) and are all transmitted in urban cycles by the same species of mosquitoes. However, YFV and DENV have been rarely reported to cause congenital diseases. Here, we compared infection with a contemporary ZIKV strain (FSS13025) to YFV17D and DENV-4 in human monocytic cells (THP-1) and first-trimester trophoblasts (HTR-8). Our results suggest that all three viruses have similar tropisms for both cells. Nevertheless, ZIKV induced strong type 1 IFN and inflammatory cytokine and chemokine production in monocytes and peripheral blood mononuclear cells. Furthermore, ZIKV infection in trophoblasts induced lower IFN and higher inflammatory immune responses. Placental inflammation is known to contribute to the risk of brain damage in preterm newborns. Inhibition of toll-like receptor (TLR)3 and TLR8 each abrogated the inflammatory cytokine responses in ZIKV-infected trophoblasts. Our findings identify a potential link between maternal immune activation and ZIKV-induced congenital diseases, and a potential therapeutic strategy that targets TLR-mediated inflammatory responses in the placenta.

Indexed as

Cells, CulturedCytokinesDengue VirusFemaleFlavivirus InfectionsGene ExpressionHumansLeukocytes, MononuclearMonocytesPregnancyPregnancy Trimester, FirstRNA, Small InterferingSpecies SpecificityToll-Like ReceptorsTrophoblastsYellow fever virusCytokinesRNA, Small InterferingToll-Like ReceptorsFlavivirusImmunityTrophoblastZika virus

Identifiers

PMID29331320
PMCPMC5844857
OpenAlexW2783688231

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.