Evidence map›Paper›PMID 29634758›Full record

ArticlePLoS pathogens2018

Zika virus infection in immunocompetent pregnant mice causes fetal damage and placental pathology in the absence of fetal infection.

Frank M Szaba, Michael Tighe, Lawrence W Kummer, Kathleen G Lanzer, Jerrold M Ward, Paula Lanthier, In-Jeong Kim, Atsuo Kuki, Marcia A Blackman, Stephen J Thomas and 1 more

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 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
14.2field-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

69 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Maternal Immune Activation: Implications for Congenital Heart Defects.Clinical reviews in allergy & immunology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. The Innate Defense in the Zika-Infected Placenta.Pathogens (Basel, Switzerland) · 2022
    Review
  20. Article

9 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

11 authors at 3 institutions in 1 country.

Frank M SzabaTrudeau Institute, Saranac Lake, New York, United States of America.
Michael TigheTrudeau Institute, Saranac Lake, New York, United States of America.ORCID 0000-0003-3679-5688
Lawrence W KummerTrudeau Institute, Saranac Lake, New York, United States of America.
Kathleen G LanzerTrudeau Institute, Saranac Lake, New York, United States of America.ORCID 0000-0002-3315-8547
Jerrold M WardGlobal VetPathology, Montgomery Village, Maryland, United States of America.ORCID 0000-0002-6350-8982
Paula LanthierTrudeau Institute, Saranac Lake, New York, United States of America.
In-Jeong KimTrudeau Institute, Saranac Lake, New York, United States of America.
Atsuo KukiTrudeau Institute, Saranac Lake, New York, United States of America.
Marcia A BlackmanTrudeau Institute, Saranac Lake, New York, United States of America.ORCID 0000-0002-6106-7490
Stephen J ThomasUpstate Medical University, State University of New York, Syracuse, New York, United States of America.
Jr-Shiuan LinTrudeau Institute, Saranac Lake, New York, United States of America.ORCID 0000-0003-0583-148X
Trudeau Institute · USGlobal VetPathology · USSUNY Upstate Medical University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zika virus (ZIKV) infection during human pregnancy may cause diverse and serious congenital defects in the developing fetus. Previous efforts to generate animal models of human ZIKV infection and clinical symptoms often involved manipulating mice to impair their Type I interferon (IFN) signaling, thereby allowing enhanced infection and vertical transmission of virus to the embryo. Here, we show that even pregnant mice competent to generate Type I IFN responses that can limit ZIKV infection nonetheless develop profound placental pathology and high frequency of fetal demise. We consistently found that maternal ZIKV exposure led to placental pathology and that ZIKV RNA levels measured in maternal, placental or embryonic tissues were not predictive of the pathological effects seen in the embryos. Placental pathology included trophoblast hyperplasia in the labyrinth, trophoblast giant cell necrosis in the junctional zone, and loss of embryonic vessels. Our findings suggest that, in this context of limited infection, placental pathology rather than embryonic/fetal viral infection may be a stronger contributor to adverse pregnancy outcomes in mice. Our finding demonstrates that in immunocompetent mice, direct viral infection of the embryo is not essential for fetal demise. Our immunologically unmanipulated pregnancy mouse model provides a consistent and easily measurable congenital abnormality readout to assess fetal outcome, and may serve as an additional model to test prophylactic and therapeutic interventions to protect the fetus during pregnancy, and for studying the mechanisms of ZIKV congenital immunopathogenesis.

Indexed as

Disease Models, AnimalAnimalsFemaleFetal DiseasesInfectious Disease Transmission, VerticalMiceMice, Inbred C57BLPlacenta DiseasesPregnancyPregnancy Complications, InfectiousPregnancy OutcomeRNA, ViralZika VirusZika Virus InfectionRNA, Viral

Identifiers

PMID29634758
PMCPMC5909921
OpenAlexW2797004612

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.