Evidence map›Paper›PMID 20864677›Full record

ArticleThe American journal of pathology2010

Toll-like receptor (TLR) 2 and TLR9 expressed in trigeminal ganglia are critical to viral control during herpes simplex virus 1 infection.

Graciela Kunrath Lima, Guilherme Pimenta Zolini, Daniel Santos Mansur, Bráulio Henrique Freire Lima, Uschi Wischhoff, Ruiz Gerhardt Astigarraga, Marcela França Dias, Mariana das Graças Almeida Silva, Samantha Ribeiro Béla, Lis Ribeiro do Valle Antonelli and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
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  9. Review
  10. Article
  11. Article
  12. Review
  13. Evasion of Intracellular DNA Sensing by Human Herpesviruses.Frontiers in cellular and infection microbiology · 2021
    Review
  14. Review
  15. Article
  16. Mechanisms of Blood-Brain Barrier Disruption in Herpes Simplex Encephalitis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Review
  17. Review
  18. Herpes Simplex Virus Evasion of Early Host Antiviral Responses.Frontiers in cellular and infection microbiology · 2019
    Review
  19. Insights into the pathogenesis of herpes simplex encephalitis from mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  20. Article
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

15 authors at 3 institutions in 2 countries.

Graciela Kunrath LimaDepartamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Laboratório de Imunopatologia, CPqRR/FIOCRUZ. Av. Augusto de Lima, 1715. CEP: 30.190-002 Belo Horizonte, MG, Brazil.
Guilherme Pimenta Zolini
Daniel Santos Mansur
Bráulio Henrique Freire Lima
Uschi Wischhoff
Ruiz Gerhardt Astigarraga
Marcela França Dias
Mariana das Graças Almeida Silva
Samantha Ribeiro Béla
Lis Ribeiro do Valle Antonelli
Rosa Maria Arantes
Ricardo Tostes Gazzinelli
André Báfica
Erna Geessien Kroon
Marco Antônio Campos
Fundação Oswaldo Cruz · BRUniversidade Federal de Minas Gerais · BRUniversidade Federal de Santa Catarina · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Herpes simplex virus 1 (HSV-1) is a neurotropic DNA virus that is responsible for several clinical manifestations in humans, including encephalitis. HSV-1 triggers toll-like receptors (TLRs), which elicit cytokine production. Viral multiplication and cytokine expression in C57BL/6 wild-type (WT) mice infected with HSV-1 were evaluated. Virus was found in the trigeminal ganglia (TG), but not in the brains of animals without signs of encephalitis, between 2 and 6 days postinfection (d.p.i.). Cytokine expression in the TG peaked at 5 d.p.i. TLR9-/- and TLR2/9-/- mice were more susceptible to the virus, with 60% and 100% mortality, respectively, as opposed to 10% in the WT and TLR2-/- mice. Increased levels of both CXCL10/IP-10 and CCL2/MCP-1, as well as reduced levels of interferon-γ and interleukin 1-β transcripts, measured in both the TG and brains at 5 d.p.i., and the presence of virus in the brain were correlated with total mortality in TLR2/9-/- mice. Cytokine alterations in TLR2/9-/- mice coincided with histopathological changes in their brains, which did not occur in WT and TLR2-/- mice and occurred only slightly in TLR9-/- mouse brain. Increased cellularity, macrophages, CD8 T cells producing interferon-γ, and expression levels of TLR2 and TLR9 were detected in the TG of WT-infected mice. We hypothesize that HSV-1 infection is controlled by TLR-dependent immune responses in the TG, which prevent HSV-1 encephalitis.

Indexed as

AnimalsBrainCell LineChemokinesCytokinesHerpes SimplexHerpesvirus 1, HumanHumansInterleukin-12 Subunit p40MiceMice, Inbred C57BLMice, KnockoutToll-Like Receptor 2Toll-Like Receptor 9Trigeminal GanglionTumor Necrosis Factor-alphaChemokinesCytokinesInterleukin-12 Subunit p40Toll-Like Receptor 2Toll-Like Receptor 9Tumor Necrosis Factor-alpha

Identifiers

PMID20864677
PMCPMC2966801
OpenAlexW2138854304

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.