Evidence map›Paper›PMID 20702619›Full record

ArticleJournal of virology2010

Neuropeptide Y has a protective role during murine retrovirus-induced neurological disease.

Min Du, Niranjan B Butchi, Tyson Woods, Timothy W Morgan, Karin E Peterson

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 22% 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, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  9. SARM1, Not MyD88, Mediates TLR7/TLR9-Induced Apoptosis in Neurons.Journal of immunology (Baltimore, Md. : 1950) · 2015
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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 2 institutions in 1 country.

Min DuLaboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, 903 S. 4th St., Hamilton, MT 59840, USA.
Niranjan B Butchi
Tyson Woods
Timothy W Morgan
Karin E Peterson
National Institute of Allergy and Infectious Diseases · USLouisiana State University · US

Funding

Mechanisms of Viral Pathogenesis in the Central Nervous SystemZIAAI001102 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI PETERSON, KARIN · 2009 to 2025
$16.8M
TNF AND MCP-1 IN RETROVIRUS-INDUCED BRAIN DISEASEP20RR020159 · NCRR · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI PAHAR, BAPI · 2004 to 2011
$16.1M
Intramural NIH HHSNCIRD CDC HHS IP20RR020159NCRR NIH HHS P20 RR020159
6 · The paper itself

Abstract

Viral infections in the central nervous system (CNS) can lead to neurological disease either directly by infection of neurons or indirectly through activation of glial cells and production of neurotoxic molecules. Understanding the effects of virus-mediated insults on neuronal responses and neurotrophic support is important in elucidating the underlying mechanisms of viral diseases of the CNS. In the current study, we examined the expression of neurotrophin- and neurotransmitter-related genes during infection of mice with neurovirulent polytropic retrovirus. In this model, virus-induced neuropathogenesis is indirect, as the virus predominantly infects macrophages and microglia and does not productively infect neurons or astrocytes. Virus infection is associated with glial cell activation and the production of proinflammatory cytokines in the CNS. In the current study, we identified increased expression of neuropeptide Y (NPY), a pleiotropic growth factor which can regulate both immune cells and neuronal cells, as a correlate with neurovirulent virus infection. Increased levels of Npy mRNA were consistently associated with neurological disease in multiple strains of mice and were induced only by neurovirulent, not avirulent, virus infection. NPY protein expression was primarily detected in neurons near areas of virus-infected cells. Interestingly, mice deficient in NPY developed neurological disease at a faster rate than wild-type mice, indicating a protective role for NPY. Analysis of NPY-deficient mice indicated that NPY may have multiple mechanisms by which it influences virus-induced neurological disease, including regulating the entry of virus-infected cells into the CNS.

Indexed as

RetroviridaeAnimalsGene Expression RegulationMiceNervous System DiseasesNeuronsNeuropeptide YProtective AgentsRNA, MessengerNeuropeptide YProtective AgentsRNA, Messenger

Identifiers

PMID20702619
PMCPMC2953205
OpenAlexW2139882603

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.