Evidence map›Paper›PMID 18199636›Full record

ArticleJournal of virology2008

Influenza A virus strains differ in sensitivity to the antiviral action of Mx-GTPase.

Jan Dittmann, Silke Stertz, Daniel Grimm, John Steel, Adolfo García-Sastre, Otto Haller, Georg Kochs

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Human MX1 orchestrates the cytoplasmic sequestration of neosynthesized influenza A virus vRNPs.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Antiviral Mx proteins have an ancient origin and widespread distribution among eukaryotes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Observational
  19. Article
  20. Article

28 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

7 authors at 2 institutions in 2 countries.

Jan DittmannDepartment of Virology, University of Freiburg, Hermann-Herder-Strasse 11, 79107 Freiburg, Germany.
Silke Stertz
Daniel Grimm
John Steel
Adolfo García-Sastre
Otto Haller
Georg Kochs
University of Freiburg · DEIcahn School of Medicine at Mount Sinai · US

Funding

Viral and Host cDNA Libraries from 1918 Influenza CasesP01AI058113 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GARCIA-SASTRE, ADOLFO · 2004 to 2010
$20.3M
VIRULENCE FACTORS OF INFLUENZA VIRUS--THE NS1 PROTEINR01AI046954 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GARCIA-SASTRE, ADOLFO · 2000 to 2010
$3.1M
NIAID NIH HHS P01 AI058113NIAID NIH HHS P01AI58113NIAID NIH HHS R01 AI046954NIAID NIH HHS R01AI46954
6 · The paper itself

Abstract

Interferon-mediated host responses are of great importance for controlling influenza A virus infections. It is well established that the interferon-induced Mx proteins possess powerful antiviral activities toward most influenza viruses. Here we analyzed a range of influenza A virus strains for their sensitivities to murine Mx1 and human MxA proteins and found remarkable differences. Virus strains of avian origin were highly sensitive to Mx1, whereas strains of human origin showed much weaker responses. Artificial reassortments of the viral components in a minireplicon system identified the viral nucleoprotein as the main target structure of Mx1. Interestingly, the recently reconstructed 1918 H1N1 "Spanish flu" virus was much less sensitive than the highly pathogenic avian H5N1 strain A/Vietnam/1203/04 when tested in a minireplicon system. Importantly, the human 1918 virus-based minireplicon system was almost insensitive to inhibition by human MxA, whereas the avian influenza A virus H5N1-derived system was well controlled by MxA. These findings suggest that Mx proteins provide a formidable hurdle that hinders influenza A viruses of avian origin from crossing the species barrier to humans. They further imply that the observed insensitivity of the 1918 virus-based replicon to the antiviral activity of human MxA is a hitherto unrecognized characteristic of the "Spanish flu" virus that may contribute to the high virulence of this unusual pandemic strain.

Indexed as

AnimalsCell LineChick EmbryoDogsGTP-Binding ProteinsInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H5N1 SubtypeMiceMyxovirus Resistance ProteinsNucleocapsid ProteinsNucleoproteinsReassortant VirusesRNA-Binding ProteinsRNA-Dependent RNA PolymeraseViral Core ProteinsViral Plaque AssayGTP-Binding ProteinsMX1 protein, humanMx1 protein, mouseMyxovirus Resistance ProteinsNP protein, Influenza A virusNucleocapsid ProteinsNucleoproteinsRNA-Binding ProteinsRNA-Dependent RNA PolymeraseViral Core ProteinsViral ProteinsVirulence Factors

Identifiers

PMID18199636
PMCPMC2268464
OpenAlexW2169382411

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.