Evidence map›Paper›PMID 17409090›Full record

ArticleGenetics2007

High frequency of mutations that expand the host range of an RNA virus.

Martin T Ferris, Paul Joyce, Christina L Burch

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 132 citations in OpenAlex.

  1. Article
  2. Genomic analysis ofVirus evolution · 2026
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  6. Review
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  14. Variation Profile of the Orthotospovirus Genome.Pathogens (Basel, Switzerland) · 2020
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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

3 authors at 2 institutions in 1 country.

Martin T FerrisDepartment of Biology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Paul Joyce
Christina L Burch
University of North Carolina at Chapel Hill · USUniversity of Idaho · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability of a virus population to colonize a novel host is predicted to depend on the equilibrium frequency of potential colonists (i.e., genotypes capable of infecting the novel host) in the source population. In this study, we investigated the determinants of the equilibrium frequency of potential colonists in the RNA bacteriophage 6. We isolated 40 spontaneous mutants capable of infecting a novel Pseudomonas syringae host and sequenced their host attachment genes to identify the responsible mutations. We observed 16 different mutations in the host attachment gene and used a new statistical approach to estimate that 39 additional mutations were missed by our screen. Phenotypic and fitness assays confirmed that the proximate mechanism underlying host range expansion was an increase in the ability to attach to the novel host and that acquisition of this ability most often imposed a cost for growth rate on two standard hosts. Considered in a population genetic framework, our data suggest that host range mutations should exist in phage populations at an equilibrium frequency (3 x 10(-4)) that exceeds the phage mutation rate by more than two orders of magnitude. Thus, colonization of novel hosts is unlikely to be limited by an inability to produce appropriate mutations.

Indexed as

MutationBacteriophage phi 6Cloning, MolecularKineticsPolymerase Chain ReactionPseudomonas syringaeRNA, Double-StrandedRNA PhagesRNA, ViralTranscription, GeneticViral Plaque AssayRNA, Double-StrandedRNA, Viral

Identifiers

PMID17409090
PMCPMC1894571
OpenAlexW2144802497

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.