Evidence map›Paper›PMID 24955107›Full record

ArticleFuture virology2013

The inflammasome as a target of modulation by DNA viruses.

Lisi Amsler, Daniel Malouli, Victor DeFilippis

Abstract read
In one paragraph

Article in Future virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. 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

3 authors.

Lisi Amsler *Vaccine & Gene Therapy Institute, Oregon Health & Science University, 505, NW 185th Avenue, Beaverton, OR 97006, USA.
Daniel Malouli *Vaccine & Gene Therapy Institute, Oregon Health & Science University, 505, NW 185th Avenue, Beaverton, OR 97006, USA.
Victor DeFilippisVaccine & Gene Therapy Institute, Oregon Health & Science University, 505, NW 185th Avenue, Beaverton, OR 97006, USA.

Funding

The Burden of Chikungunya and Dengue Infection in KenyaU54AI081680 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI LANDFEAR, SCOTT M · 2009 to 2013
$40.4M
Program in Molecular and Cellular BiosciencesT32GM071338 · NIGMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI MASLEN, CHERYL L · 2005 to 2020
$3.5M
Modulation of Innate Immune Responses by CytomegalovirusR01AI070890 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI FRUH, KLAUS J · 2008 to 2012
$2.4M
NIAID NIH HHS R01 AI070890NIAID NIH HHS U54 AI081680NIGMS NIH HHS T32 GM071338
6 · The paper itself

Abstract

The cellular innate immune response represents the initial reaction of a host against infecting pathogens. Host cells detect incoming microbes by way of a large and expanding array of receptors that react with evolutionarily conserved molecular patterns exhibited by microbial intruders. These receptors are responsible for initiating signaling that leads to both transcriptional activation of immunologically important genes as well as protease-dependent processing of cellular proteins. The inflammasome refers to a protein complex that functions as an activation platform for the cysteine protease caspase-1, which then processes inflammatory molecules such as IL-1β and IL-18 into functional forms. Assembly of this complex is triggered following receptor-mediated detection of pathogen-associated molecules. Receptors have been identified that are essential to inflammasome activation in response to numerous molecular patterns including virus-associated molecules such as DNA. In fact, the importance of cytoplasmic DNA as an immune stimulus is exemplified by the existence of at least nine distinct cellular receptors capable of initiating innate reactivity in response to this molecule. Viruses that employ DNA as genomic material include herpesviruses, poxviruses and adenoviruses. Each has been described as capable of inducing inflammasome-mediated activity. Interestingly, however, the cellular molecules responsible for these responses appear to vary according to host species, cell type and even viral strain. Secretion of IL-1β and IL-18 are important components of antimicrobial immunity and, as a result, pathogens have evolved factors to evade or counteract this response. This includes DNA-based viruses, many of which encode multiple redundant counteractive molecules. However, it is clear that such phenotypes are only beginning to be uncovered. The purpose of this review is to describe what is known regarding the activation of inflammasome-mediated processes in response to infection with well-examined families of DNA viruses and to discuss characterized mechanisms of manipulation and neutralization of inflammasome-dependent activity. This review aims to shed light on the biologically important phenomena regarding this virus-host interaction and to highlight key areas where important information is lacking.

Indexed as

adenoviruscaspase-1herpesvirusIL-18IL-1βimmunomodulationinflammasomeinflammationinnate immunitypoxvirus

Identifiers

PMID24955107
PMCPMC4061697

What OpenQuestion holds

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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.