Evidence map›Paper›PMID 17349048›Full record

ArticleVirology journal2007

Transplacental murine cytomegalovirus infection in the brain of SCID mice.

Nigel K Woolf, Dawn V Jaquish, Fred J Koehrn

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  7. Mouse Models for Human Herpesviruses.Pathogens (Basel, Switzerland) · 2023
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  12. 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

3 authors at 1 institution in 1 country.

Nigel K WoolfDepartments of Surgery/Anatomy, University of California Medical School at San Diego Life, 9500 Gilman Drive, La Jolla, CA 92093-0604, USA. nwoolf@ucsd.edu
Dawn V Jaquish
Fred J Koehrn
VA San Diego Healthcare System · US

Funding

CONGENITAL CYTOMEGALOVIRUS MODEL OF AUDITORY PATHOLOGYR01DC000386 · NIDCD · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI WOOLF, NIGEL KEITH · 1989 to 2005
$1.5M
CMV LABYRINTHITIS INDUCED IN IMMUNODEFICIENT SCID MICER01DC002666 · NIDCD · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI WOOLF, NIGEL KEITH · 1995 to 2004
$934k
NIDCD NIH HHS DC00386NIDCD NIH HHS DC02666NIDCD NIH HHS R01 DC000386NIDCD NIH HHS R01 DC002666
6 · The paper itself

Abstract

backgroundCongenital cytomegalovirus (CMV) infection is the most common congenital viral infection in humans and the major nonhereditary cause of central nervous system (CNS) developmental disorders. Previous attempts to develop a murine CMV (MCMV) model of natural congenital human CMV (HCMV) infection have failed because MCMV does not cross the placenta in immunocompetent mice.

resultsIn marked contrast with immunocompetent mice, C.B-17 SCID (severe combined immunodeficient) mice were found to be highly susceptible to natural MCMV transplacental transmission and congenital infection. Timed-pregnant SCID mice were intraperitoneally (IP) injected with MCMV at embryonic (E) stages E0-E7, and vertical MCMV transmission was evaluated using nested polymerase chain reaction (nPCR), in situ hybridization (ISH) and immunohistochemical (IHC) assays. SCID mouse dams IP injected at E0 with 102 PFU of MCMV died or resorbed their fetuses by E18. Viable fetuses collected at E18 from SCID mice IP injected with 102-104 PFU of MCMV at E7 did not demonstrate vertical MCMV transmission. Notably, transplacental MCMV transmission was confirmed in E18 fetuses from SCID mice IP injected with 103 PFU of MCMV at stages E3-E5. The maximum rate of transplacental MCMV transmission (53%) at E18 occurred when SCID mouse dams were IP injected with 103 PFU of MCMV at E4. Congenital infection was confirmed by IHC immunostaining of MCMV antigens in 26% of the MCMV nPCR positive E18 fetuses. Transplacental MCMV transmission was associated with intrauterine growth retardation and microcephaly. Additionally, E18 fetuses with MCMV nPCR positive brains had cerebral interleukin-1alpha (IL-1alpha) expression significantly upregulated and cerebral IL-1 receptor II (IL-1RII) transcription significantly downregulated. However, MCMV-induced changes in cerebral cytokine expression were not associated with any histological signs of MCMV infection or inflammation in the brain.

conclusionSevere T- and B-cell immunodeficiencies in SCID mice significantly enhance the rate of natural MCMV transplacental transmission and congenital infection. During gestation MCMV exhibits a tissue tropism for the developing brain, and vertical MCMV transmission is correlated with fetal growth retardation and abnormal cerebral proinflammatory cytokine expression. These data confirm that natural vertical MCMV infection in SCID mice constitutes a useful new experimental rodent model of congenital HCMV infection.

Indexed as

Disease Models, AnimalMice, SCIDAnimalsAnimals, NewbornBrainCentral Nervous System Viral DiseasesCytomegalovirus InfectionsFemaleFetal DiseasesHumansInfectious Disease Transmission, VerticalMaleMiceMuromegalovirusPlacentaPregnancy

Identifiers

PMID17349048
PMCPMC1838414
OpenAlexW1996664062

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.