Evidence map›Paper›PMID 24778238›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Genesis and pathogenesis of the 1918 pandemic H1N1 influenza A virus.

Michael Worobey, Guan-Zhu Han, Andrew Rambaut

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 2 pooled it
13.7field-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

153 citing papers in PubMed, 2 syntheses or guidelines pooled it, 284 citations in OpenAlex.

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93 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 3 countries.

Michael WorobeyDepartment of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721; worobey@email.arizona.edu.
Guan-Zhu HanDepartment of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721;
Andrew RambautInstitute of Evolutionary Biology andCentre for Infection, Immunity, and Evolution, University of Edinburgh, Edinburgh EH9 3JT, United Kingdom; andFogarty International Center, National Institutes of Health, Bethesda, MD 20892.
University of Arizona · USUniversity of Edinburgh · GB

Funding

Molecular Archeology of HIVR01AI084691 · NIAID · UNIVERSITY OF ARIZONA · PI WOROBEY, MICHAEL · 2011 to 2014
$1.2M
European Research Council 260864NIAID NIH HHS R01 AI084691Wellcome Trust 092807Wellcome Trust 095831
6 · The paper itself

Abstract

The source, timing, and geographical origin of the 1918-1920 pandemic influenza A virus have remained tenaciously obscure for nearly a century, as have the reasons for its unusual severity among young adults. Here, we reconstruct the origins of the pandemic virus and the classic swine influenza and (postpandemic) seasonal H1N1 lineages using a host-specific molecular clock approach that is demonstrably more accurate than previous methods. Our results suggest that the 1918 pandemic virus originated shortly before 1918 when a human H1 virus, which we infer emerged before ∼1907, acquired avian N1 neuraminidase and internal protein genes. We find that the resulting pandemic virus jumped directly to swine but was likely displaced in humans by ∼1922 by a reassortant with an antigenically distinct H1 HA. Hence, although the swine lineage was a direct descendent of the pandemic virus, the post-1918 seasonal H1N1 lineage evidently was not, at least for HA. These findings help resolve several seemingly disparate observations from 20th century influenza epidemiology, seroarcheology, and immunology. The phylogenetic results, combined with these other lines of evidence, suggest that the high mortality in 1918 among adults aged ∼20 to ∼40 y may have been due primarily to their childhood exposure to a doubly heterosubtypic putative H3N8 virus, which we estimate circulated from ∼1889-1900. All other age groups (except immunologically naive infants) were likely partially protected by childhood exposure to N1 and/or H1-related antigens. Similar processes may underlie age-specific mortality differences between seasonal H1N1 vs. H3N2 and human H5N1 vs. H7N9 infections.

Indexed as

AdultAgedAnimalsBiological EvolutionBirdsChildDisease ResistanceGenetic VariationHumansInfluenza A virusInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H3N2 SubtypeInfluenza A Virus, H3N8 SubtypeInfluenza A Virus, H5N1 SubtypeInfluenza A Virus, H7N9 SubtypeInfluenza, Humancohort immunitypathogenicityphylogenyreassortmentvirulence

Identifiers

PMID24778238
PMCPMC4050607
OpenAlexW2068005913

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.