Evidence map›Paper›PMID 21423754›Full record

ArticlePloS one2011

Human papillomavirus deregulates the response of a cellular network comprising of chemotactic and proinflammatory genes.

Rezaul Karim, Craig Meyers, Claude Backendorf, Kristina Ludigs, Rienk Offringa, Gert-Jan B van Ommen, Cornelis J M Melief, Sjoerd H van der Burg, Judith M Boer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing 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

90 citing papers in PubMed, 156 citations in OpenAlex.

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30 more citing papers are in PubMed but not listed here.

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 5 institutions in 3 countries.

Rezaul KarimCenter for Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Craig Meyers
Claude Backendorf
Kristina Ludigs
Rienk Offringa
Gert-Jan B van Ommen
Cornelis J M Melief
Sjoerd H van der Burg
Judith M Boer
Leiden University Medical Center · NLLaboratory of Molecular Genetics · PLLeiden University · NLNetherlands Bioinformatics Centre · NLPenn State Milton S. Hershey Medical Center · US

Funding

Genetic Analysis of Papillomavirus Virion MorphogenesisR01AI057988 · NIAID · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI MEYERS, CRAIG M · 2006 to 2009
$1.4M
NIAID NIH HHS AI057988NIAID NIH HHS R01 AI057988
6 · The paper itself

Abstract

Despite the presence of intracellular pathogen recognition receptors that allow infected cells to attract the immune system, undifferentiated keratinocytes (KCs) are the main targets for latent infection with high-risk human papilloma viruses (hrHPVs). HPV infections are transient but on average last for more than one year suggesting that HPV has developed means to evade host immunity. To understand how HPV persists, we studied the innate immune response of undifferentiated human KCs harboring episomal copies of HPV16 and 18 by genome-wide expression profiling. Our data showed that the expression of the different virus-sensing receptors was not affected by the presence of HPV. Poly(I:C) stimulation of the viral RNA receptors TLR3, PKR, MDA5 and RIG-I, the latter of which indirectly senses viral DNA through non-self RNA polymerase III transcripts, showed dampening in downstream signalling of these receptors by HPVs. Many of the genes downregulated in HPV-positive KCs involved components of the antigen presenting pathway, the inflammasome, the production of antivirals, pro-inflammatory and chemotactic cytokines, and components downstream of activated pathogen receptors. Notably, gene and/or protein interaction analysis revealed the downregulation of a network of genes that was strongly interconnected by IL-1β, a crucial cytokine to activate adaptive immunity. In summary, our comprehensive expression profiling approach revealed that HPV16 and 18 coordinate a broad deregulation of the keratinocyte's inflammatory response, and contributes to the understanding of virus persistence.

Indexed as

AnimalsCells, CulturedChemotaxisDown-RegulationGene Regulatory NetworksGenes, ViralHumansInflammasomesInflammation MediatorsInterleukin-1betaKeratinocytesMicePapillomaviridaePoly I-CReceptors, VirusUp-RegulationInflammasomesInflammation MediatorsInterleukin-1betaPoly I-CReceptors, Virus

Identifiers

PMID21423754
PMCPMC3056770
OpenAlexW1967040249

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.