Evidence map›Paper›PMID 16501082›Full record

ArticleJournal of virology2006

Feline lentivirus evolution in cross-species infection reveals extensive G-to-A mutation and selection on key residues in the viral polymerase.

Mary Poss, Howard A Ross, Sally L Painter, David C Holley, Julie A Terwee, Sue Vandewoude, Allen Rodrigo

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
9.4field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Mary PossDivision of Biological Sciences, HS104, University of Montana, Missoula, Montana 59812, USA. mary.poss@umontana.edu
Howard A Ross
Sally L Painter
David C Holley
Julie A Terwee
Sue Vandewoude
Allen Rodrigo
Colorado State University · USUniversity of Auckland · NZUniversity of Montana · US

Funding

Understanding the molecular mechanism of pathogenesis of prion diseasesP20RR015583 · NCRR · UNIVERSITY OF MONTANA · PI KAVANAUGH, MICHAEL PATRICK · 2000 to 2009
$17.6M
Mechanisms of Feline Lentivirus Control and InterferenceR01AI052055 · NIAID · COLORADO STATE UNIVERSITY-FORT COLLINS · PI VANDEWOUDE, SUE · 2002 to 2005
$1.4M
Characterization of cougar lentivirusesR15AI054303 · NIAID · UNIVERSITY OF MONTANA · PI POSS, MARY L. · 2003 to 2003
$140k
NCRR NIH HHS P20 RR015583NCRR NIH HHS P20 RR15583-01NIAID NIH HHS AI 052055NIAID NIH HHS AI 054303NIAID NIH HHS R01 AI052055NIAID NIH HHS R15 AI054303
6 · The paper itself

Abstract

Factors that restrict a virus from establishing productive infection in a new host species are important to understand because cross-species transmission events are often associated with emergent viral diseases. To determine the evolutionary pressures on viruses in new host species, we evaluated the molecular evolution of a feline immunodeficiency virus derived from a wild cougar, Puma concolor, during infection of domestic cats. Analyses were based on the coding portion of genome sequences recovered at intervals over 37 weeks of infection of six cats inoculated by either intravenous or oral-nasal routes. All cats inoculated intravenously, but only one inoculated orally-nasally, became persistently viremic. There were notable accumulations of lethal errors and predominance of G-to-A alterations throughout the genome, which were marked in the viral polymerase gene, pol. Viral structural (env and gag) and accessory (vif and orfA) genes evolved neutrally or were under purifying selection. However, sites under positive selection were identified in reverse transcriptase that involved residues in the nucleotide binding pocket or those contacting the RNA-DNA duplex. The findings of extensive G-to-A alterations in this cross-species infection are consistent with the recently described editing of host cytidine deaminase on lentivirus genomes. Additionally, we demonstrate that the primary site of hypermutation is the viral pol gene and the dominant selective force acting on this feline immunodeficiency virus as it replicates in a new host species is on key residues of the virus polymerase.

Indexed as

Evolution, MolecularGenes, polMutationSelection, GeneticAnimalsAnimals, DomesticCat DiseasesCatsFeline Acquired Immunodeficiency SyndromeImmunodeficiency Virus, FelineModels, MolecularMolecular Sequence DataPhylogenyPumaSequence Analysis, DNASpecies Specificity

Identifiers

PMID16501082
PMCPMC1395431
OpenAlexW2123451223

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.