Evidence map›Paper›PMID 28539439›Full record

ArticleJournal of virology2017

Contribution of Human Lung Parenchyma and Leukocyte Influx to Oxidative Stress and Immune System-Mediated Pathology following Nipah Virus Infection.

Olivier Escaffre, Tais B Saito, Terry L Juelich, Tetsuro Ikegami, Jennifer K Smith, David D Perez, Colm Atkins, Corri B Levine, Matthew B Huante, Rebecca J Nusbaum and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. 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
1.0field-weighted citation impact, top 23% 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, 16 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

13 authors at 1 institution in 2 countries.

Olivier EscaffreDepartment of Pathology, University of Texas Medical Branch, Galveston, Texas, USA.
Tais B SaitoDepartment of Pathology, University of Texas Medical Branch, Galveston, Texas, USA.
Terry L JuelichDepartment of Pathology, University of Texas Medical Branch, Galveston, Texas, USA.
Tetsuro IkegamiDepartment of Pathology, University of Texas Medical Branch, Galveston, Texas, USA.
Jennifer K SmithDepartment of Pathology, University of Texas Medical Branch, Galveston, Texas, USA.
David D PerezDepartment of Pathology, University of Texas Medical Branch, Galveston, Texas, USA.
Colm AtkinsDepartment of Pathology, University of Texas Medical Branch, Galveston, Texas, USA.
Corri B LevineInstitute for Translational Sciences, University of Texas Medical Branch, Galveston, Texas, USA.
Matthew B HuanteDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA.
Rebecca J NusbaumDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA.
Janice J EndsleyDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA.
Alexander N FreibergDepartment of Pathology, University of Texas Medical Branch, Galveston, Texas, USA anfreibe@utmb.edu b.rockx@erasmusmc.nl.
Barry RockxDepartment of Pathology, University of Texas Medical Branch, Galveston, Texas, USA anfreibe@utmb.edu b.rockx@erasmusmc.nl.
The University of Texas Medical Branch at Galveston · US

Funding

Role of Reactive Oxygen Species in Nipah Virus PathogenesisR21AI111042 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI FREIBERG, ALEXANDER NICLAS · 2014 to 2015
$426k
NIAID NIH HHS R21 AI111042
6 · The paper itself

Abstract

Nipah virus (NiV) is a zoonotic emerging paramyxovirus that can cause fatal respiratory illness or encephalitis in humans. Despite many efforts, the molecular mechanisms of NiV-induced acute lung injury (ALI) remain unclear. We previously showed that NiV replicates to high titers in human lung grafts in NOD-SCID/γ mice, resulting in a robust inflammatory response. Interestingly, these mice can undergo human immune system reconstitution by the bone marrow, liver, and thymus (BLT) reconstitution method, in addition to lung tissue engraftment, giving altogether a realistic model to study human respiratory viral infections. Here, we characterized NiV Bangladesh strain (NiV-B) infection of human lung grafts from human immune system-reconstituted mice in order to identify the overall effect of immune cells on NiV pathogenesis of the lung. We show that NiV-B replicated to high titers in human lung grafts and caused similar cytopathic effects irrespective of the presence of human leukocytes in mice. However, the human immune system interfered with virus spread across lung grafts, responded to infection by leukocyte migration to small airways and alveoli of the lung grafts, and accelerated oxidative stress in lung grafts. In addition, the presence of human leukocytes increased the expression of cytokines and chemokines that regulate inflammatory influx to sites of infection and tissue damage. These results advance our understanding of how the immune system limits NiV dissemination and contributes to ALI and inform efforts to identify therapeutic targets.

Indexed as

Oxidative StressAcute Lung InjuryAnimalsCytokinesDisease Models, AnimalHenipavirus InfectionsHumansLeukocytesLungMiceMice, SCIDNipah VirusCytokinesantioxidant therapieshenipavirushumanized mousehuman lung graftsinflammatory responseoxidative stressvirus replication

Identifiers

PMID28539439
PMCPMC5651721
OpenAlexW2619491552

What OpenQuestion holds

Textmetadata
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.