Evidence map›Paper›PMID 33824206›Full record

ArticlemBio2021

Gammaherpesvirus Usurps Host IL-17 Signaling To Support the Establishment of Chronic Infection.

C N Jondle, K E Johnson, C Aurubin, P Sylvester, G Xin, W Cui, A R Huppler, V L Tarakanova

Open access · goldAbstract read
In one paragraph

Article in mBio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 23 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

8 authors at 3 institutions in 1 country.

C N JondleDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA cjondle@mcw.edu vera@mcw.edu.
K E JohnsonDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
C AurubinDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
P SylvesterDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
G XinBlood Research Institute, Versiti, Milwaukee, Wisconsin, USA.
W CuiBlood Research Institute, Versiti, Milwaukee, Wisconsin, USA.
A R HupplerDepartment of Pediatrics, Children's Hospital of Wisconsin Research Institute, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
V L TarakanovaDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA cjondle@mcw.edu vera@mcw.edu.ORCID 0000-0002-9499-088X
Medical College of Wisconsin · USVersiti Blood Center of Wisconsin · USChildren's Hospital of Wisconsin · US

Funding

Medical Scientist Training ProgramT32GM080202 · NIGMS · MEDICAL COLLEGE OF WISCONSIN · PI BARBIERI, JOSEPH T, SALZMAN, NITA H · 2010 to 2024
$5.7M
IRF-1: a brake to limit gammaherpesvirus infection and pathogenesisR01CA203923 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI TARAKANOVA, VERA L. · 2017 to 2021
$2.0M
Anti-Candida activity of CCL28 in oropharyngeal candidiasisK08DE026189 · NIDCR · MEDICAL COLLEGE OF WISCONSIN · PI HUPPLER, ANNA · 2017 to 2021
$860k
The tale of two receptors: Determining the role of lipoprotein receptors, SR-BI and LDL-R, in gammaherpesvirus infectionF30CA247000 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI AURUBIN, CARLIE ANNE · 2020 to 2023
$176k
Not just acute: IRF-7 has two site-specific functions against chronic gammaherpesvirus infectionF31CA243364 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI JOHNSON, KAITLIN E · 2019 to 2020
$45k
NCI NIH HHS F30 CA247000NCI NIH HHS F31 CA243364NCI NIH HHS R01 CA203923NIDCR NIH HHS K08 DE026189NIGMS NIH HHS T32 GM080202
6 · The paper itself

Abstract

Gammaherpesviruses establish lifelong infection and are associated with a variety of cancers, including B cell lymphomas. These viruses manipulate the B cell differentiation process to establish lifelong infection in memory B cells. Specifically, gammaherpesviruses infect naive B cells and promote entry of both infected and uninfected naive B cells into germinal centers, where the virus usurps rapid proliferation of germinal center B cells to exponentially increase its cellular latent reservoir. In addition to facilitating the establishment of latent infection, germinal center B cells are thought to be the target of viral transformation. In this study, we have uncovered a novel proviral role of host interleukin 17A (IL-17A), a well-established antibacterial and antifungal factor. Loss of IL-17A signaling attenuated the establishment of chronic gammaherpesvirus infection and gammaherpesvirus-driven germinal center response in a route of inoculation-dependent manner. Further, IL-17A treatment directly supported gammaherpesvirus reactivation and

Indexed as

AnimalsCells, CulturedChronic DiseaseFemaleGammaherpesvirinaeHerpesviridae InfectionsHost-Pathogen InteractionsInterleukin-17MacrophagesMaleMiceMice, Inbred C57BLSignal TransductionIl17a protein, mouseInterleukin-17chronic infectiongammaherpesvirusgerminal center responseIL-17 signaling

Identifiers

PMID33824206
PMCPMC8092251
OpenAlexW3142707093

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.