Evidence map›Paper›PMID 24710494›Full record

ArticleCells2012

Virus-heat shock protein interaction and a novel axis for innate antiviral immunity.

Mi Young Kim, Michael Oglesbee

Open access · goldAbstract read
In one paragraph

Article in Cells, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

27 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Orsay virus infection increasesBiology letters · 2024
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. HSP70iCell stress & chaperones · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Assessing the oncolytic potential of rotavirus on mouse myeloma cell line Sp2/0-Ag14.Biomedica : revista del Instituto Nacional de Salud · 2020
    Article
  16. Review
  17. Evaluation of Disease Severity and Global Transcriptome Response Induced byInternational journal of molecular sciences · 2019
    Article
  18. Chaperoning theViruses · 2018
    Review
  19. Article
  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

2 authors at 1 institution in 1 country.

Mi Young KimDepartment of Veterinary Biosciences, The Ohio State University, 1925 Coffey Road, Columbus, OH 43210, USA. kim.2612@osu.edu.
Michael OglesbeeDepartment of Veterinary Biosciences, The Ohio State University, 1925 Coffey Road, Columbus, OH 43210, USA. Michael.Oglesbee@cvm.osu.edu.
The Ohio State University · US

Funding

THE CELLULAR STRESS RESPONSE IN VIRAL ENCEPHALITISR01NS031693 · NINDS · OHIO STATE UNIVERSITY · PI OGLESBEE, MICHAEL J · 2000 to 2008
$1.8M
Heat shock protein modulation of paramyxoviral diseaseR21AI071174 · NIAID · OHIO STATE UNIVERSITY · PI OGLESBEE, MICHAEL J · 2008 to 2009
$413k
NIAID NIH HHS R21 AI071174NINDS NIH HHS R01 NS031693
6 · The paper itself

Abstract

Virus infections induce heat shock proteins that in turn enhance virus gene expression, a phenomenon that is particularly well characterized for the major inducible 70 kDa heat shock protein (hsp70). However, hsp70 is also readily induced by fever, a phylogenetically conserved response to microbial infections, and when released from cells, hsp70 can stimulate innate immune responses through toll like receptors 2 and 4 (TLR2 and 4). This review examines how the virus-hsp70 relationship can lead to host protective innate antiviral immunity, and the importance of hsp70 dependent stimulation of virus gene expression in this host response. Beginning with the well-characterized measles virus-hsp70 relationship and the mouse model of neuronal infection in brain, we examine data indicating that the innate immune response is not driven by intracellular sensors of pathogen associated molecular patterns, but rather by extracellular ligands signaling through TLR2 and 4. Specifically, we address the relationship between virus gene expression, extracellular release of hsp70 (as a damage associated molecular pattern), and hsp70-mediated induction of antigen presentation and type 1 interferons in uninfected macrophages as a novel axis of antiviral immunity. New data are discussed that examines the more broad relevance of this protective mechanism using vesicular stomatitis virus, and a review of the literature is presented that supports the probable relevance to both RNA and DNA viruses and for infections both within and outside of the central nervous system.

Identifiers

PMID24710494
PMCPMC3901102
OpenAlexW2021204404

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.