Evidence map›Paper›PMID 30814283›Full record

ArticleJournal of virology2019

NK Cells Accumulate in Infected Tissues and Contribute to Pathogenicity of Ebola Virus in Mice.

H Fausther-Bovendo, X Qiu, S He, A Bello, J Audet, G Ippolito, G Wong, G Kobinger

Open access · hybridAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 34 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 2 institutions in 3 countries.

H Fausther-BovendoNational Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Canada.
X QiuNational Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Canada.
S HeNational Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Canada.
A BelloNational Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Canada.
J AudetNational Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Canada.
G IppolitoNational Institute for Infectious Diseases, Lazzaro Spallanzani, National Institute for Infectious Diseases-IRCCS, Rome, Italy.
G WongNational Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Canada.
G KobingerNational Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Canada Gary.Kobinger@crchudequebec.ulaval.ca.ORCID 0000-0003-0612-2298
Public Health Agency of Canada · CAIstituto Nazionale per le Malattie Infettive Lazzaro Spallanzani · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding the immune parameters responsible for survival following Ebola virus (EBOV) infection is paramount for developing countermeasures. In lethal EBOV infections, levels of both NK and T cells decline drastically in the circulation and lymphoid tissues before death. However, the fate of these lymphocytes in viral replication sites remains unknown. In this study, reverse transcription-PCR (RT-PCR) and fluorescence-activated cell sorting (FACS) analysis were used to investigate lymphocyte frequencies in various infected mouse tissues after challenge with mouse-adapted EBOV (MA-EBOV). A decrease in NK cell numbers from systemic circulation was observed concomitant to an increase of these cells in tissues that are supporting active replication of EBOV. Unexpectedly, NK accumulation in virus replication sites correlated with enhanced EBOV disease progression in specific conditions; at a high challenge dose, NK-depleted mice displayed lower viremia and liver damage and higher hepatic T cell levels. Upregulation of UL16 binding protein 1 (ULBP-1) was detected in hepatic T cells, suggesting that NK cells participate in their elimination. Overall, this study supports the concept that NK cells accumulate in EBOV-infected tissues and can contribute to viral pathogenicity.

Indexed as

AnimalsCytokinesDisease Models, AnimalDisease ProgressionEbolavirusFemaleHemorrhagic Fever, EbolaHistocompatibility Antigens Class IKiller Cells, NaturalLymphocytesMembrane ProteinsMiceMice, Inbred BALB CMice, Inbred C57BLT-LymphocytesVirulenceCytokinesHistocompatibility Antigens Class IMembrane ProteinsUL16 binding protein 1, mouseautologous killingEbola viruslymphopeniaNK cellsULBP-1

Identifiers

PMID30814283
PMCPMC6498052
OpenAlexW2916272305

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.