Evidence map›Paper›PMID 30377281›Full record

ArticlemBio2018

Structural and Nonstructural Genes Contribute to the Genetic Diversity of RNA Viruses.

Natalie D Collins, Andrew S Beck, Steven G Widen, Thomas G Wood, Stephen Higgs, Alan D T Barrett

Open access · goldAbstract read
In one paragraph

Article in mBio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  4. Unraveling flavivirus pathogenesis: from bulk to single-cell RNA-sequencing strategies.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
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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

6 authors at 2 institutions in 1 country.

Natalie D CollinsDepartment of Microbiology & Immunology, University of Texas Medical Branch, Galveston, Texas, USA.
Andrew S BeckDepartment of Pathology, University of Texas Medical Branch, Galveston, Texas, USA.
Steven G WidenMolecular Genomics Core Facility, University of Texas Medical Branch, Galveston, Texas, USA.
Thomas G WoodMolecular Genomics Core Facility, University of Texas Medical Branch, Galveston, Texas, USA.
Stephen HiggsDepartment of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, Kansas, USA.
Alan D T BarrettDepartment of Microbiology & Immunology, University of Texas Medical Branch, Galveston, Texas, USA abarrett@utmb.edu.
The University of Texas Medical Branch at Galveston · USKansas State University · US

Funding

Next Generation sequencing of yellow fever 17D vaccine virusR21AI113407 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI BARRETT, ALAN D.T. · 2015 to 2016
$426k
NIAID NIH HHS R21 AI113407
6 · The paper itself

Abstract

One paradigm to explain the complexity of viral RNA populations is that the low fidelity of the RNA-dependent RNA polymerase (RdRp) drives high mutation rates and consequently genetic diversity. Like most RNA viruses, wild-type yellow fever virus (YFV) replication is error-prone due to the lack of proofreading by the virus-encoded RdRp. However, there is evidence that replication of the live attenuated YF vaccine virus 17D, derived from wild-type strain Asibi, is less error-prone than wild-type RNA viruses. Recent studies comparing the genetic diversity of wild-type Asibi and 17D vaccine virus found that wild-type Asibi has the typical heterogeneous population of an RNA virus, while there is limited intra- and interpopulation variability of 17D vaccine virus. Utilizing chimeric and mutant infectious clone-derived viruses, we show that high and low genetic diversity profiles of wild-type Asibi virus and vaccine virus 17D, respectively, are multigenic. Introduction of either structural (pre-membrane and envelope) genes or NS2B or NS4B substitutions into the Asibi and 17D backbone resulted in altered variant population, nucleotide diversity, and mutation frequency compared to the parental viruses. Additionally, changes in genetic diversity of the chimeric and mutant viruses correlated with the phenotype of multiplication kinetics in human alveolar A549 cells. Overall, the paradigm that only the error-prone RdRp controls genetic diversity needs to be expanded to address the role of other genes in genetic diversity, and we hypothesize that it is the replication complex as a whole and not the RdRp alone that controls genetic diversity.

Indexed as

Genetic VariationA549 CellsHumansMutation RateRecombination, GeneticReverse GeneticsViral Nonstructural ProteinsViral Structural ProteinsYellow fever virusViral Nonstructural ProteinsViral Structural ProteinsattenuationdiversityRNA virusesvaccineviral populationyellow fever

Identifiers

PMID30377281
PMCPMC6212827
OpenAlexW2899155229

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.