Evidence map›Paper›PMID 17537853›Full record

ArticleJournal of virology2007

Interferon-mediated immunopathological events are associated with atypical innate and adaptive immune responses in patients with severe acute respiratory syndrome.

Mark J Cameron, Longsi Ran, Luoling Xu, Ali Danesh, Jesus F Bermejo-Martin, Cheryl M Cameron, Matthew P Muller, Wayne L Gold, Susan E Richardson, Susan M Poutanen and 17 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 260 papers.

0numbers the graph read from it
0cells of the map it votes in
260citing papers in PubMed
8.9field-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

260 citing papers in PubMed, 405 citations in OpenAlex.

  1. Review
  2. Article
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  4. Article
  5. Human coronaviruses: activation and antagonism of innate immune responses.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  6. Anti-interferon armamentarium of human coronaviruses.Cellular and molecular life sciences : CMLS · 2025
    Review
  7. Review
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200 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

27 authors at 8 institutions in 2 countries.

Mark J CameronDivision of Experimental Therapeutics, University Health Network, MaRS Centre, 3-916 TMDT, 101 College Street, Toronto, Ontario, Canada.
Longsi Ran
Luoling Xu
Ali Danesh
Jesus F Bermejo-Martin
Cheryl M Cameron
Matthew P Muller
Wayne L Gold
Susan E Richardson
Susan M Poutanen
Barbara M Willey
Mark E DeVries
Yuan Fang
Charit Seneviratne
Steven E Bosinger
Desmond Persad
Peter Wilkinson
Larry D Greller
Roland Somogyi
Atul Humar
Shaf Keshavjee
Marie Louie
Mark B Loeb
James Brunton
Allison J McGeer
Canadian SARS Research Network
David J Kelvin
University Health Network · CAUniversity of Toronto · CAMount Sinai Hospital · CAHôpital Saint-Luc · CAMcMaster University · CAProvincial Laboratory of Public Health · CAToronto Public Health · CAUniversidad de Valladolid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is not understood how immune inflammation influences the pathogenesis of severe acute respiratory syndrome (SARS). One area of strong controversy is the role of interferon (IFN) responses in the natural history of SARS. The fact that the majority of SARS patients recover after relatively moderate illness suggests that the prevailing notion of deficient type I IFN-mediated immunity, with hypercytokinemia driving a poor clinical course, is oversimplified. We used proteomic and genomic technology to systematically analyze host innate and adaptive immune responses of 40 clinically well-described patients with SARS during discrete phases of illness from the onset of symptoms to discharge or a fatal outcome. A novel signature of high IFN-alpha, IFN-gamma, and IFN-stimulated chemokine levels, plus robust antiviral IFN-stimulated gene (ISG) expression, accompanied early SARS sequelae. As acute illness progressed, SARS patients entered a crisis phase linked to oxygen saturation profiles. The majority of SARS patients resolved IFN responses at crisis and expressed adaptive immune genes. In contrast, patients with poor outcomes showed deviated ISG and immunoglobulin gene expression levels, persistent chemokine levels, and deficient anti-SARS spike antibody production. We contend that unregulated IFN responses during acute-phase SARS may culminate in a malfunction of the switch from innate immunity to adaptive immunity. The potential for the use of the gene signatures we describe in this study to better assess the immunopathology and clinical management of severe viral infections, such as SARS and avian influenza (H5N1), is therefore worth careful examination.

Indexed as

Gene Expression ProfilingAdultAgedAged, 80 and overAntibodies, ViralAntibody FormationCytokinesFemaleGene ExpressionGenomicsHumansImmunity, InnateInterferonsMaleMiddle AgedOligonucleotide Array Sequence AnalysisAntibodies, ViralCytokinesInterferons

Identifiers

PMID17537853
PMCPMC1951379
OpenAlexW2049902839

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.