Evidence map›Paper›PMID 21880769›Full record

ArticleJournal of virology2011

Adaptive and innate transforming growth factor beta signaling impact herpes simplex virus 1 latency and reactivation.

Sariah J Allen, Kevin R Mott, Steven L Wechsler, Richard A Flavell, Terrence Town, Homayon Ghiasi

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact, top 85% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

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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

6 authors at 3 institutions in 1 country.

Sariah J AllenCenter for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery and Regenerative Medicine Institute, Los Angeles, California 90048, USA.
Kevin R Mott
Steven L Wechsler
Richard A Flavell
Terrence Town
Homayon Ghiasi
Howard Hughes Medical Institute · USUniversity of California, Irvine · USUniversity of California, Los Angeles · US

Funding

The Role of gK in HSV-1 Induced Corneal ScarringR01EY013615 · NEI · CEDARS-SINAI MEDICAL CENTER · PI HOMAYON GHIASI · 2002 to 2026
$7.8M
Corneal HSV-1: LAT's Anti-Apoptosis Activity and LatencyR01EY013191 · NEI · UNIVERSITY OF CALIFORNIA-IRVINE · PI WECHSLER, STEVEN L · 2001 to 2013
$6.9M
Ocular HSV: Role of virus and IL-2 in Optic neuritisR01EY015557 · NEI · CEDARS-SINAI MEDICAL CENTER · PI GHIASI, HOMAYON · 2006 to 2010
$1.7M
The Cedars-Sinai Immunobiology Training ProgramT32AI089553 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE, TARGAN, STEPHAN R. · 2010 to 2016
$1.1M
Innate &adaptive immunities in control of ocular HSVR01EY014966 · NEI · CEDARS-SINAI MEDICAL CENTER · PI GHIASI, HOMAYON · 2005 to 2007
$1.0M
Howard Hughes Medical InstituteNEI NIH HHS EY013191NEI NIH HHS EY13615NEI NIH HHS EY15557NEI NIH HHS R01 EY013191NEI NIH HHS R01 EY013615NEI NIH HHS R01 EY014966NEI NIH HHS R01 EY015557NIAID NIH HHS 1T32AI089553NIAID NIH HHS T32 AI089553
6 · The paper itself

Abstract

Innate and adaptive immunity play important protective roles by combating herpes simplex virus 1 (HSV-1) infection. Transforming growth factor β (TGF-β) is a key negative cytokine regulator of both innate and adaptive immune responses. Yet, it is unknown whether TGF-β signaling in either immune compartment impacts HSV-1 replication and latency. We undertook genetic approaches to address these issues by infecting two different dominant negative TGF-β receptor type II transgenic mouse lines. These mice have specific TGF-β signaling blockades in either T cells or innate cells. Mice were ocularly infected with HSV-1 to evaluate the effects of restricted innate or adaptive TGF-β signaling during acute and latent infections. Limiting innate cell but not T cell TGF-β signaling reduced virus replication in the eyes of infected mice. On the other hand, blocking TGF-β signaling in either innate cells or T cells resulted in decreased latency in the trigeminal ganglia of infected mice. Furthermore, inhibiting TGF-β signaling in T cells reduced cell lysis and leukocyte infiltration in corneas and trigeminal ganglia during primary HSV-1 infection of mice. These findings strongly suggest that TGF-β signaling, which generally functions to dampen immune responses, results in increased HSV-1 latency.

Indexed as

Gene Expression Regulation, ViralSignal TransductionVirus ActivationVirus LatencyAnimalsDisease Models, AnimalEyeHerpesvirus 1, HumanKeratitis, HerpeticMiceMice, TransgenicRodent DiseasesTransforming Growth Factor betaTrigeminal GanglionVirus ReplicationTransforming Growth Factor beta

Identifiers

PMID21880769
PMCPMC3194985
OpenAlexW2105850171

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.