Evidence map›Paper›PMID 25198371›Full record

ArticlePediatric research2014

Herpes simplex virus serotype and entry receptor availability alter CNS disease in a mouse model of neonatal HSV.

Sarah J Kopp, Hantamalala R Ranaivo, Douglas R Wilcox, Andrew H Karaba, Mark S Wainwright, William J Muller

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Pediatric research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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  11. Innate Immune Mechanisms and Herpes Simplex Virus Infection and Disease.Advances in anatomy, embryology, and cell biology · 2017
    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

6 authors at 1 institution in 1 country.

Sarah J Kopp1] Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Illinois [2] Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Hantamalala R RanaivoDepartment of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Douglas R Wilcox1] Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Illinois [2] Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Andrew H KarabaDepartment of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Mark S WainwrightDepartment of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
William J MullerDepartment of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Northwestern University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM008152 · NIGMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ARDEHALI, HOSSEIN · 1987 to 2021
$24.0M
Herpes Simplex Virus Entry Receptors in Immune Memory and Newborn InfectionK08AI089942 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MULLER, WILLIAM JOSEPH · 2010 to 2012
$387k
NIAID NIH HHS K08 AI089942NIAID NIH HHS K08AI089942NIGMS NIH HHS T32 GM008152
6 · The paper itself

Abstract

backgroundOutcomes of neonates with herpes simplex virus (HSV) encephalitis are worse after infection with HSV-2 when compared with HSV-1. The proteins herpes virus entry mediator (HVEM) and nectin-1 mediate HSV entry into susceptible cells. Prior studies have shown receptor-dependent differences in pathogenesis that depend on route of inoculation and host developmental age.

methodsWe investigated serotype-related differences in HSV disease and their relationship to entry receptor availability in a mouse model of encephalitis.

resultsMortality was attenuated in 7-d-old, wild-type (WT) mice inoculated with HSV-1(F) when compared with HSV-2(333). No serotype-specific differences were seen after inoculation of adult mice. HSV-1 pathogenesis was also attenuated relative to HSV-2 in newborn but not adult mice lacking HVEM or nectin-1. HSV-2 requires nectin-1 for encephalitis in adult but not newborn mice; in contrast, nectin-1 was important for HSV-1 pathogenesis in both age groups. Early viral replication was independent of age, viral serotype, or mouse genotype, suggesting host responses influence outcomes. In this regard, significantly greater amounts of inflammatory mediators were detected in brain homogenates from WT newborns 2 d after infection compared with adults and receptor-knockout newborns.

conclusionDysregulation of inflammatory responses induced by infection may influence the severity of HSV encephalitis.

Indexed as

Virus InternalizationAnimalsAnimals, NewbornCell Adhesion MoleculesDisease Models, AnimalEncephalitis, Herpes SimplexGenotypeHerpes SimplexHerpesvirus 1, HumanHerpesvirus 2, HumanHost-Pathogen InteractionsInflammation MediatorsMiceMice, Inbred C57BLMice, KnockoutNectinsCell Adhesion MoleculesInflammation MediatorsNECTIN1 protein, humanNectin1 protein, mouseNectinsReceptors, Tumor Necrosis Factor, Member 14Tnfrsf14 protein, mouse

Identifiers

PMID25198371
PMCPMC4233006
OpenAlexW1964345128

What OpenQuestion holds

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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.