Evidence map›Paper›PMID 31725732›Full record

ArticlePloS one2019

Mechanisms of African swine fever virus pathogenesis and immune evasion inferred from gene expression changes in infected swine macrophages.

James J Zhu, Palaniappan Ramanathan, Elizabeth A Bishop, Vivian O'Donnell, Douglas P Gladue, Manuel V Borca

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
17.2field-weighted citation impact, top 1% 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

75 citing papers in PubMed, 116 citations in OpenAlex.

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15 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

6 authors at 3 institutions in 1 country.

James J ZhuUSDA-ARS, FADRU, Plum Island Animal Disease Center, Orient, New York, United States of America.
Palaniappan RamanathanOak Ridge Institute for Science and Education (ORISE), Oak Ridge, Tennessee, United States of America.ORCID 0000-0001-8121-7647
Elizabeth A BishopUSDA-ARS, FADRU, Plum Island Animal Disease Center, Orient, New York, United States of America.
Vivian O'DonnellUSDA-APHIS, Plum Island Animal Disease Center, Orient, New York, United States of America.
Douglas P GladueUSDA-ARS, FADRU, Plum Island Animal Disease Center, Orient, New York, United States of America.ORCID 0000-0002-7894-0233
Manuel V BorcaUSDA-ARS, FADRU, Plum Island Animal Disease Center, Orient, New York, United States of America.
Plum Island Animal Disease Center · USAnimal and Plant Health Inspection Service · USOak Ridge Associated Universities · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

African swine fever (ASF) is a swine disease caused by a large, structurally complex, double-stranded DNA virus, African swine fever virus (ASFV). In domestic pigs, acute infection by highly virulent ASF viruses causes hemorrhagic fever and death. Previous work has suggested that ASFV pathogenesis is primarily mediated by host cytokines produced by infected monocytes and macrophages. To better understand molecular mechanisms mediating virus pathogenesis and immune evasion, we used transcriptome analysis to identify gene expression changes after ASFV infection in ex vivo swine macrophages. Our results suggest that the cytokines of TNF family including FASLG, LTA, LTB, TNF, TNFSF4, TNFSF10, TNFSF13B and TNFSF18 are the major causative cytokine factors in ASF pathogenesis via inducing apoptosis. Other up-regulated proinflammatory cytokines (IL17F and interferons) and down-regulated anti-inflammatory cytokine (IL10) may also significantly contribute to ASF pathogenesis and cause excessive tissue inflammatory responses. The differential expression of genes also indicates that ASFV could evade both the innate and adaptive immune responses by (i) inhibiting MHC Class II antigen processing and presentation, (ii) avoiding CD8+ T effector cells and neutrophil extracellular traps via decreasing expression of neutrophil/CD8+ T effector cell-recruiting chemokines, (iii) suppressing M1 activation of macrophages, (iv) inducing immune suppressive cytokines, and (v) inhibiting the processes of macrophage autophagy and apoptosis. These results provide novel information to further investigate and better understand the mechanism of pathogenesis and immune evasion of this devastating swine disease.

Indexed as

Immune EvasionAdaptive ImmunityAfrican Swine FeverAfrican Swine Fever VirusAnimalsAntigen PresentationAutophagy-Related ProteinsCells, CulturedChemokinesCytokinesDown-RegulationGene Expression ProfilingImmunity, InnateMacrophage ActivationMacrophagesReceptors, CytokineAutophagy-Related ProteinsChemokinesCytokinesReceptors, Cytokine

Identifiers

PMID31725732
PMCPMC6855437
OpenAlexW2983874376

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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 OpenQuestion graph.