Evidence map›Paper›PMID 28806913›Full record

ArticleBMC genomics2017

Proteomics informed by transcriptomics for characterising differential cellular susceptibility to Nelson Bay orthoreovirus infection.

Lawrence Mok, James W Wynne, Mary Tachedjian, Brian Shiell, Kris Ford, David A Matthews, Antony Bacic, Wojtek P Michalski

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

4 citing papers in PubMed, 6 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 4 institutions in 2 countries.

Lawrence MokCSIRO, Australian Animal Health Laboratory, East Geelong, VIC, Australia.
James W WynneCSIRO, Australian Animal Health Laboratory, East Geelong, VIC, Australia. james.wynne@csiro.au.
Mary TachedjianCSIRO, Australian Animal Health Laboratory, East Geelong, VIC, Australia.
Brian ShiellCSIRO, Australian Animal Health Laboratory, East Geelong, VIC, Australia.
Kris FordARC Centre of Excellence in Plant Cell Walls School of BioSciences, The University of Melbourne, Melbourne, VIC, Australia.
David A MatthewsDepartment of Cellular and Molecular Medicine, School of Medical Sciences, University of Bristol, Bristol, UK.
Antony BacicARC Centre of Excellence in Plant Cell Walls School of BioSciences, The University of Melbourne, Melbourne, VIC, Australia.
Wojtek P MichalskiCSIRO, Australian Animal Health Laboratory, East Geelong, VIC, Australia.
Australian Centre for Disease Preparedness · AUARC Centre of Excellence in Plant Energy Biology · AUCommonwealth Scientific and Industrial Research Organisation · AUUniversity of Bristol · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNelson Bay orthoreovirus (NBV) is a fusogenic bat borne virus with an unknown zoonotic potential. Previous studies have shown that NBV can infect and replicate in a wide variety of cell types derived from their natural host (bat), as well as from human, mouse and monkey. Within permissive cells, NBV induced significant cytopathic effects characterised by cell-cell fusion and syncytia formation. To understand the molecular events that underpin NBV infection we examined the host transcriptome and proteome response of two cell types, derived from bat (PaKiT03) and mouse (L929), to characterise differential cellular susceptibility to NBV.

resultsDespite significant differences in NBV replication and cytopathic effects in the L929 and PaKiT03 cells, the host response was remarkably similar in these cells. At both the transcriptome and proteome level, the host response was dominated by IFN production and signalling pathways. The majority of proteins up-regulated in L929 and PaKiT03 cells were also up-regulated at the mRNA (gene) level, and included many important IFN stimulated genes. Further functional experimentation demonstrated that stimulating IFN signalling prior to infection, significantly reduced NBV replication in PaKiT03 cells. Moreover, inhibiting IFN signalling (through specific siRNAs) increased NBV replication in L929 cells. In line with the significant cytopathic effects seen in PaKiT03 cells, we also observed a down-regulation of genes involved in cell-cell junctions, which may be related to the fusogenic effects of NBV.

conclusionsThis study provides new multi-dimensional insights into the host response of mammalian cells to NBV infection. We show that IFN activity is capable of reducing NBV replication, although it is unlikely that this is solely responsible for the reduced replication of NBV in L929 cells. The molecular events that underpin the fusogenic cytopathic effects described here will prove valuable for identifying potential therapeutic targets against fusogenic orthoreovirus.

Indexed as

Gene Expression ProfilingProteomicsAnimalsCell LineChiropteraInterferonsMiceOrthoreovirusRNA, MessengerSignal TransductionVirus ReplicationInterferonsRNA, MessengerHostImmuneInterferonNelson bayOrthoreovirusPITProteomicsProteomics informed by transcriptomicsResponseTranscriptomics

Identifiers

PMID28806913
PMCPMC5556373
OpenAlexW2750296736

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.