Evidence map›Paper›PMID 31250000›Full record

ArticleThe Journal of infectious diseases2020

Zika Virus Nonstructural Protein 1 Disrupts Glycosaminoglycans and Causes Permeability in Developing Human Placentas.

Henry Puerta-Guardo, Takako Tabata, Matthew Petitt, Milena Dimitrova, Dustin R Glasner, Lenore Pereira, Eva Harris

Open access · greenAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

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  7. Dengue Virus NS1 Binds Ephrin B1 to Trigger Endothelial Dysfunction.bioRxiv : the preprint server for biology · 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

7 authors at 2 institutions in 1 country.

Henry Puerta-GuardoDivision of Infectious Diseases and Vaccinology, School of Public Health, University of California, Berkeley.
Takako TabataDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco.
Matthew PetittDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco.
Milena DimitrovaDivision of Infectious Diseases and Vaccinology, School of Public Health, University of California, Berkeley.
Dustin R GlasnerDivision of Infectious Diseases and Vaccinology, School of Public Health, University of California, Berkeley.
Lenore PereiraDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco.
Eva HarrisDivision of Infectious Diseases and Vaccinology, School of Public Health, University of California, Berkeley.
University of California, Berkeley · USUniversity of California, San Francisco · US

Funding

Dissecting novel mechanisms of dengue virus NS1-induced vascular leakR01AI124493 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI HARRIS, EVA · 2016 to 2020
$1.9M
Fetal Zika virus infection: role of the human placentaR21AI129508 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HARRIS, EVA, PEREIRA, LENORE PALMA · 2017 to 2018
$435k
NIAID NIH HHS R01 AI124493NIAID NIH HHS R21 AI129508
6 · The paper itself

Abstract

backgroundDuring pregnancy, the Zika flavivirus (ZIKV) infects human placentas, inducing defects in the developing fetus. The flavivirus nonstructural protein 1 (NS1) alters glycosaminoglycans on the endothelium, causing hyperpermeability in vitro and vascular leakage in vivo in a tissue-dependent manner. The contribution of ZIKV NS1 to placental dysfunction during ZIKV infection remains unknown.

methodsWe examined the effect of ZIKV NS1 on expression and release of heparan sulfate (HS), hyaluronic acid (HA), and sialic acid on human trophoblast cell lines and anchoring villous explants from first-trimester placentas infected with ZIKV ex vivo. We measured changes in permeability in trophoblasts and stromal cores using a dextran-based fluorescence assay and changes in HA receptor expression using immunofluorescent microscopy.

resultsZIKV NS1 in the presence and absence of ZIKV increased the permeability of anchoring villous explants. ZIKV NS1 induced shedding of HA and HS and altered expression of CD44 and lymphatic endothelial cell HA receptor-1, HA receptors on stromal fibroblasts and Hofbauer macrophages in villous cores. Hyaluronidase was also stimulated in NS1-treated trophoblasts.

conclusionsThese findings suggest that ZIKV NS1 contributes to placental dysfunction via modulation of glycosaminoglycans on trophoblasts and chorionic villi, resulting in increased permeability of human placentas.

Indexed as

FemaleGlycosaminoglycansHumansInfectious Disease Transmission, VerticalPermeabilityPlacentaPregnancyPregnancy Complications, InfectiousViral Nonstructural ProteinsZika VirusZika Virus InfectionGlycosaminoglycansNS1 protein, zika virusViral Nonstructural Proteinscytotrophoblastheparan sulfateHofbauer cellshyaluronic acidZika virus NS1

Identifiers

PMID31250000
PMCPMC6936002
OpenAlexW2954978558

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.