Evidence map›Paper›PMID 27638253›Full record

ArticleThe American journal of pathology2016

Persistent Cytomegalovirus Infection in Amniotic Membranes of the Human Placenta.

Takako Tabata, Matthew Petitt, June Fang-Hoover, Martin Zydek, Lenore Pereira

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

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  11. Trophoblastic extracellular vesicles and viruses: Friends or foes?American journal of reproductive immunology (New York, N.Y. : 1989) · 2021
    Review
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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

5 authors at 1 institution in 1 country.

Takako TabataDepartment of Cell and Tissue Biology, School of Dentistry, University of California, San Francisco, San Francisco, California.
Matthew PetittDepartment of Cell and Tissue Biology, School of Dentistry, University of California, San Francisco, San Francisco, California.
June Fang-HooverDepartment of Cell and Tissue Biology, School of Dentistry, University of California, San Francisco, San Francisco, California.
Martin ZydekDepartment of Cell and Tissue Biology, School of Dentistry, University of California, San Francisco, San Francisco, California.
Lenore PereiraDepartment of Cell and Tissue Biology, School of Dentistry, University of California, San Francisco, San Francisco, California. Electronic address: lenore.pereira@ucsf.edu.
University of California, San Francisco · US

Funding

Fetal HCMV Infection: Role of the Human PlacentaR01AI046657 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PEREIRA, LENORE PALMA · 2000 to 2017
$5.9M
HCMV infection of human placental trophoblast and hematopoietic progenitorsR56AI101130 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PEREIRA, LENORE PALMA · 2012 to 2012
$546k
The role of CEACAM1 in CMV pathogenesis in the human placentaR21HD061890 · NICHD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TABATA, TAKAKO · 2011 to 2012
$415k
NIAID NIH HHS R01 AI046657NIAID NIH HHS R56 AI101130NICHD NIH HHS R21 HD061890
6 · The paper itself

Abstract

Human cytomegalovirus (HCMV) is the leading viral cause of birth defects, including microcephaly, neurological deficits, hearing impairment, and vision loss. We previously reported that epithelial cells in amniotic membranes of placentas from newborns with intrauterine growth restriction and underlying congenital HCMV infection contain viral proteins in cytoplasmic vesicles. Herein, we immunostained amniotic membranes from 51 placentas from symptomatic and asymptomatic congenital infection with HCMV DNA in amniotic fluid and/or newborn saliva, intrauterine growth restriction, preterm deliveries, and controls. We consistently observed HCMV proteins in amniotic epithelial cells (AmEpCs) from infected placentas, sometimes with aberrant morphology. Primary AmEpCs isolated from mid-gestation placentas infected with pathogenic VR1814 proliferated and released infectious progeny for weeks, producing higher virus titers than late-gestation cells that varied by donor. In contrast to intact virion assembly compartments in differentiated retinal pigment epithelial cells, infected AmEpCs made dispersed multivesicular bodies. Primary AmEpCs and explants of amniochorionic membranes from mid-gestation placentas formed foci of infection, and interferon-β production was prolonged. Infected AmEpCs up-regulated anti-apoptotic proteins survivin and Bcl-x

Indexed as

AmnionCytomegalovirusCytomegalovirus InfectionsFemaleFetal Growth RetardationFetusGestational AgeHumansInfant, NewbornInterferon-betaPlacentaPregnancyPregnancy Complications, InfectiousViral LoadVirus ReplicationInterferon-beta

Identifiers

PMID27638253
PMCPMC5222962
OpenAlexW2520581762

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.