Evidence map›Paper›PMID 32310998›Full record

ArticlePLoS pathogens2020

Contribution of STAT1 to innate and adaptive immunity during type I interferon-mediated lethal virus infection.

So Ri Jung, Thomas M Ashhurst, Phillip K West, Barney Viengkhou, Nicholas J C King, Iain L Campbell, Markus J Hofer

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 25 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

7 authors at 1 institution in 1 country.

So Ri JungSchool of Life and Environmental Sciences, The University of Sydney, Sydney, Australia.ORCID 0000-0003-1611-7644
Thomas M AshhurstSydney Cytometry Core Facility, The University of Sydney and Centenary Institute, Sydney, Australia.
Phillip K WestSchool of Life and Environmental Sciences, The University of Sydney, Sydney, Australia.
Barney ViengkhouSchool of Life and Environmental Sciences, The University of Sydney, Sydney, Australia.ORCID 0000-0002-1665-3060
Nicholas J C KingThe Marie Bashir Institute for Infectious Diseases and Biosecurity, the Charles Perkins Centre and the Bosch Institute, The University of Sydney, Sydney, Australia.ORCID 0000-0002-3877-9772
Iain L CampbellSchool of Life and Environmental Sciences, The University of Sydney, Sydney, Australia.
Markus J HoferSchool of Life and Environmental Sciences, The University of Sydney, Sydney, Australia.ORCID 0000-0001-5111-3978
The University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal transducers and activators of transcription (STAT) 1 is critical for cellular responses to type I interferons (IFN-Is), with the capacity to determine the outcome of viral infection. We previously showed that while wildtype (WT) mice develop mild disease and survive infection with lymphocytic choriomeningitis virus (LCMV), LCMV infection of STAT1-deficient mice results in a lethal wasting disease that is dependent on IFN-I and CD4+ cells. IFN-Is are considered to act as a bridge between innate and adaptive immunity. Here, we determined the relative contribution of STAT1 on innate and adaptive immunity during LCMV infection. We show that STAT1 deficiency results in a biphasic disease following LCMV infection. The initial, innate immunity-driven phase of disease was characterized by rapid weight loss, thrombocytopenia, systemic cytokine and chemokine responses and leukocyte infiltration of infected organs. In the absence of an adaptive immune response, this first phase of disease largely resolved resulting in survival of the infected host. However, in the presence of adaptive immunity, the disease progressed into a second phase with continued cytokine and chemokine production, persistent leukocyte extravasation into infected tissues and ultimately, host death. Overall, our findings demonstrate the key contribution of STAT1 in modulating innate and adaptive immunity during type I interferon-mediated lethal virus infection.

Indexed as

Adaptive ImmunityAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesFemaleImmunity, InnateInterferon Type ILymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionSTAT1 Transcription FactorVirus DiseasesInterferon Type IStat1 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID32310998
PMCPMC7192509
OpenAlexW3016420052

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.