Evidence map›Paper›PMID 36803114›Full record

ArticleStem cells and development2023

Activation of the Interferon Pathway in Trophoblast Cells Productively Infected with SARS-CoV-2.

Sampada Kallol, Laura Martin-Sancho, Robert Morey, Omonigho Aisagbonhi, Donald Pizzo, Morgan Meads, Sumit K Chanda, Francesca Soncin

Open access · greenAbstract read
In one paragraph

Article in Stem cells and development, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

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  5. Review
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.

Sampada KallolDepartment of Pathology; Gynecology, and Reproductive Sciences; University of California San Diego, La Jolla, California, USA.
Laura Martin-SanchoImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA.
Robert MoreyDepartment of Pathology; Gynecology, and Reproductive Sciences; University of California San Diego, La Jolla, California, USA.
Omonigho AisagbonhiDepartment of Pathology; Gynecology, and Reproductive Sciences; University of California San Diego, La Jolla, California, USA.
Donald PizzoDepartment of Pathology; Gynecology, and Reproductive Sciences; University of California San Diego, La Jolla, California, USA.
Morgan MeadsDepartment of Pathology; Gynecology, and Reproductive Sciences; University of California San Diego, La Jolla, California, USA.
Sumit K ChandaImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA.
Francesca SoncinDepartment of Pathology; Gynecology, and Reproductive Sciences; University of California San Diego, La Jolla, California, USA.ORCID 0000-0002-7423-9167
University of California San Diego · USSanford Burnham Prebys Medical Discovery Institute · US

Funding

Illumina NovaSeq 6000 Sequencing SystemS10OD026929 · OD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JEPSEN, KRISTEN LYNN · 2019 to 2019
$600k
NIH HHS S10 OD026929
6 · The paper itself

Abstract

SARS-CoV-2 infection during pregnancy has been associated with poor maternal and neonatal outcomes and placental defects. The placenta, which acts as a physical and immunological barrier at the maternal-fetal interface, is not established until the end of the first trimester. Therefore, localized viral infection of the trophoblast compartment early in gestation could trigger an inflammatory response resulting in altered placental function and consequent suboptimal conditions for fetal growth and development. In this study, we investigated the effect of SARS-CoV-2 infection in early gestation placentae using placenta-derived human trophoblast stem cells (TSCs), a novel in vitro model, and their extravillous trophoblast (EVT) and syncytiotrophoblast (STB) derivatives. SARS-CoV-2 was able to productively replicate in TSC-derived STB and EVT, but not undifferentiated TSCs, which is consistent with the expression of SARS-CoV-2 entry host factors, ACE2 (angiotensin-converting enzyme 2) and TMPRSS2 (transmembrane cellular serine protease) in these cells. In addition, both TSC-derived EVT and STB infected with SARS-CoV-2 elicited an interferon-mediated innate immune response. Combined, these results suggest that placenta-derived TSCs are a robust in vitro model to investigate the effect of SARS-CoV-2 infection in the trophoblast compartment of the early placenta and that SARS-CoV-2 infection in early gestation activates the innate immune response and inflammation pathways. Therefore, placental development could be adversely affected by early SARS-CoV-2 infection by directly infecting the developing differentiated trophoblast compartment, posing a higher risk for poor pregnancy outcomes.

Indexed as

COVID-19SARS-CoV-2FemaleHumansInfant, NewbornInterferonsPlacentaPregnancyTrophoblastsInterferonshuman placentainflammatory responseinnate immune responseSARS-CoV-2 infectiontrophoblast stem cells

Identifiers

PMID36803114
PMCPMC10171947
OpenAlexW4321335663

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.