Evidence map›Paper›PMID 26004185›Full record

ArticleCell reports2015

Mutational Analysis of Measles Virus Suggests Constraints on Antigenic Variation of the Glycoproteins.

Benjamin O Fulton, David Sachs, Shannon M Beaty, Sohui T Won, Benhur Lee, Peter Palese, Nicholas S Heaton

Abstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

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  15. Fitness selection of hyperfusogenic measles virus F proteins associated with neuropathogenic phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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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.

Benjamin O FultonDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
David SachsDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Shannon M BeatyDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Sohui T WonDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Benhur LeeDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Peter PaleseDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Nicholas S HeatonDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: nicholas.heaton@mssm.edu.

Funding

Vaccines and Diagnostics TrialsU54AI065359 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI BARBOUR, ALAN G. · 2005 to 2013
$88.8M
Toward a Universal Influenza Virus VaccineP01AI097092 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GARCIA-SASTRE, ADOLFO · 2012 to 2022
$17.6M
TRAINING PROGRAM: MECHANISMS OF VIRUS-HOST INTERACTIONST32AI007647 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI Domenico Tortorella · 2000 to 2026
$11.5M
Understanding Human B Cell Responses to Influenza to Improve the Influenza U19AI109946 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI RAVETCH, JEFFREY VICTOR · 2014 to 2018
$9.6M
Bioavailable proteasome inhibitors as broad-spectrum antiviralsR33AI102267 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI FREIBERG, ALEXANDER NICLAS · 2014 to 2016
$1.2M
Functional interrogation of paramyxovirus genomes with efficient reverse geneticsR21AI115226 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEE, BENHUR · 2015 to 2016
$460k
NIAID NIH HHS HHSN272201400008CNIAID NIH HHS P01 AI097092NIAID NIH HHS P01AI097092-02NIAID NIH HHS R21 AI115226NIAID NIH HHS R21AI115226-01NIAID NIH HHS R33 AI102267NIAID NIH HHS R33AI102267-03NIAID NIH HHS T32 AI007647NIAID NIH HHS U19 AI109946NIAID NIH HHS U19AI109946-01NIAID NIH HHS U54 AI065359NIAID NIH HHS U54AI065359PHS HHS HHSN272201400008C
6 · The paper itself

Abstract

Measles virus undergoes error-prone replication like other RNA viruses, but over time, it has remained antigenically monotypic. The constraints on the virus that prevent the emergence of antigenic variants are unclear. As a first step in understanding this question, we subjected the measles virus genome to unbiased insertional mutagenesis, and viruses that could tolerate insertions were rescued. Only insertions in the nucleoprotein, phosphoprotein, matrix protein, as well as intergenic regions were easily recoverable. Insertions in the glycoproteins of measles virus were severely under-represented in our screen. Host immunity depends on developing neutralizing antibodies to the hemagglutinin and fusion glycoproteins; our analysis suggests that these proteins occupy very little evolutionary space and therefore have difficulty changing in the face of selective pressures. We propose that the inelasticity of these proteins prevents the sequence variation required to escape antibody neutralization in the host, allowing for long-lived immunity after infection with the virus.

Indexed as

Antigenic VariationAntigens, ViralDNA Mutational AnalysisGlycoproteinsHumansMeasles virusMutagenesis, Site-DirectedTransfectionViral ProteinsAntigens, ViralGlycoproteinsViral Proteins

Identifiers

PMID26004185
PMCPMC4464907

What OpenQuestion holds

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Registered trials

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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.