Evidence map›Paper›PMID 19016073›Full record

ArticleJournal of neurovirology2008

Toll-like receptor 7 is not necessary for retroviral neuropathogenesis but does contribute to virus-induced neuroinflammation.

Stephanie D Lewis, Niranjan B Butchi, Mohammed Khaleduzzaman, Tim W Morgan, Min Du, Susan Pourciau, David G Baker, Shizuo Akira, Karin E Peterson

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neurovirology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. SARM1, Not MyD88, Mediates TLR7/TLR9-Induced Apoptosis in Neurons.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  3. Article
  4. Article
  5. Human endogenous retroviruses and the nervous system.Handbook of clinical neurology · 2014
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Toll-like receptors 3, 4, and 7 are expressed in the enteric nervous system and dorsal root ganglia.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2009
    Article
  15. 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

9 authors at 2 institutions in 2 countries.

Stephanie D LewisDepartment of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana, USA.
Niranjan B Butchi
Mohammed Khaleduzzaman
Tim W Morgan
Min Du
Susan Pourciau
David G Baker
Shizuo Akira
Karin E Peterson
Louisiana State University · USOsaka University · JP

Funding

Role of cytokines in retroviral neuropathogenesisK22AI057118 · NIAID · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI PETERSON, KARIN E · 2004 to 2005
$269k
NCIRD CDC HHS IP20RR020159NIAID NIH HHS K22AI57118-2
6 · The paper itself

Abstract

Toll-like receptor 7 (TLR7) recognizes guanidine-rich single-stranded (ss) viral RNA and is an important mediator of peripheral immune responses to several ssRNA viruses. However, the role that TLR7 plays in regulating the innate immune response to ssRNA virus infections in specific organs is not as clear. This is particularly true in the central nervous system (CNS) where microglia and astrocytes are often the first cells responding to virus infection instead of dendritic cells. In the current study, we examined the mechanism by which TLR7 contributes to ssRNA virus-induced neuroinflammation using a mouse model of polytropic retrovirus infection. The authors found that TLR7 was necessary for the early production of certain cytokines and chemokines, including CCL2 and tumor necrosis factor (TNF) and was also involved in the early activation of astrocytes. However, TLR7 was not necessary for cytokine production and astrocyte activation at later stages of infection and did not alter viral pathogenesis or viral replication in the brain. This suggests that other pathogen recognition receptors may be able to compensate for the lack of TLR7 during retrovirus infection in the CNS.

Indexed as

AnimalsAnimals, NewbornAstrocytesBrainCells, CulturedChemokine CCL2Chemokine CXCL10Disease Models, AnimalEncephalitis, ViralFemaleInterferon-betaMaleMembrane GlycoproteinsMiceMice, Inbred C57BLRetroviridaeChemokine CCL2Chemokine CXCL10Interferon-betaMembrane GlycoproteinsTlr7 protein, mouseToll-Like Receptor 7Tumor Necrosis Factor-alpha

Identifiers

PMID19016073
OpenAlexW1976183856

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.