Evidence map›Paper›PMID 31059555›Full record

ArticlePLoS pathogens2019

Kaposi's sarcoma-associated herpesvirus vIRF2 protein utilizes an IFN-dependent pathway to regulate viral early gene expression.

Sandra Koch, Modester Damas, Anika Freise, Elias Hage, Akshay Dhingra, Jessica Rückert, Antonio Gallo, Elisabeth Kremmer, Werner Tegge, Mark Brönstrup and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

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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

12 authors at 5 institutions in 1 country.

Sandra KochHannover Medical School, Institute of Virology, Hannover, Germany.ORCID 0000-0003-3759-9996
Modester DamasHannover Medical School, Institute of Virology, Hannover, Germany.
Anika FreiseHannover Medical School, Institute of Virology, Hannover, Germany.ORCID 0000-0003-3312-888X
Elias HageHannover Medical School, Institute of Virology, Hannover, Germany.
Akshay DhingraHannover Medical School, Institute of Virology, Hannover, Germany.
Jessica RückertHannover Medical School, Institute of Virology, Hannover, Germany.
Antonio GalloHeinrich-Pette-Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany.
Elisabeth KremmerInstitute of Molecular Immunology, Helmholtz Centre Munich, German Research Center for Environmental Health, Munich, Germany.ORCID 0000-0002-8133-8374
Werner TeggeHelmholtz Centre for Infection Research, Braunschweig, Germany.ORCID 0000-0003-1088-974X
Mark BrönstrupGerman Centre for Infection Research, Hannover-Braunschweig Site, Germany.ORCID 0000-0002-8971-7045
Wolfram BruneHeinrich-Pette-Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany.ORCID 0000-0002-6078-5255
Thomas F SchulzHannover Medical School, Institute of Virology, Hannover, Germany.ORCID 0000-0001-8792-5345
Medizinische Hochschule Hannover · DELeibniz Institute of Virology (LIV) · DEGerman Center for Infection Research · DEHelmholtz Centre for Infection Research · DEHelmholtz Zentrum München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV; human herpesvirus 8) belongs to the subfamily of Gammaherpesvirinae and is the etiological agent of Kaposi's sarcoma as well as of two lymphoproliferative diseases: primary effusion lymphoma and multicentric Castleman disease. The KSHV life cycle is divided into a latent and a lytic phase and is highly regulated by viral immunomodulatory proteins which control the host antiviral immune response. Among them is a group of proteins with homology to cellular interferon regulatory factors, the viral interferon regulatory factors 1-4. The KSHV vIRFs are known as inhibitors of cellular interferon signaling and are involved in different oncogenic pathways. Here we characterized the role of the second vIRF protein, vIRF2, during the KSHV life cycle. We found the vIRF2 protein to be expressed in different KSHV positive cells with early lytic kinetics. Importantly, we observed that vIRF2 suppresses the expression of viral early lytic genes in both newly infected and reactivated persistently infected endothelial cells. This vIRF2-dependent regulation of the KSHV life cycle might involve the increased expression of cellular interferon-induced genes such as the IFIT proteins 1, 2 and 3, which antagonize the expression of early KSHV lytic proteins. Our findings suggest a model in which the viral protein vIRF2 allows KSHV to harness an IFN-dependent pathway to regulate KSHV early gene expression.

Indexed as

Gene Expression Regulation, ViralVirus ActivationCells, CulturedEndothelium, VascularHerpesvirus 8, HumanHumansImmediate-Early ProteinsInterferon Regulatory FactorsInterferonsSarcoma, KaposiViral ProteinsVirus LatencyImmediate-Early ProteinsInterferon Regulatory FactorsInterferonsviral interferon regulatory factorsViral Proteins

Identifiers

PMID31059555
PMCPMC6522069
OpenAlexW2944556599

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.