Evidence map›Paper›PMID 22973048›Full record

ArticleJournal of virology2012

Constraints on viral evolution during chronic hepatitis C virus infection arising from a common-source exposure.

Justin R Bailey, Sarah Laskey, Lisa N Wasilewski, Supriya Munshaw, Liam J Fanning, Elizabeth Kenny-Walsh, Stuart C Ray

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

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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 at 3 institutions in 2 countries.

Justin R BaileyDivision of Infectious Diseases, Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.
Sarah Laskey
Lisa N Wasilewski
Supriya Munshaw
Liam J Fanning
Elizabeth Kenny-Walsh
Stuart C Ray
Office of Infectious Diseases · USNational University of Ireland · IEJohns Hopkins University · US

Funding

CELLULAR &MOLECULAR MECH OF INFLAMMATORY REACTIONST32AI007247 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Joel L Pomerantz · 1985 to 2026
$10.2M
Scientific CoreU19AI088791 · NIAID · JOHNS HOPKINS UNIVERSITY · PI COX, ANDREA L · 2010 to 2020
$8.2M
Mechanisms of Hepatitis C Virus EvolutionR01DA024565 · NIDA · JOHNS HOPKINS UNIVERSITY · PI RAY, STUART C · 2007 to 2011
$2.6M
NIAID NIH HHS T32 AI007247NIAID NIH HHS U19 AI088791NIAID NIH HHS U19 AI088791-2NIDA NIH HHS R01 DA024565
6 · The paper itself

Abstract

Extraordinary viral sequence diversity and rapid viral genetic evolution are hallmarks of hepatitis C virus (HCV) infection. Viral sequence evolution has previously been shown to mediate escape from cytotoxic T-lymphocyte (CTL) and neutralizing antibody responses in acute HCV infection. HCV evolution continues during chronic infection, but the pressures driving these changes are poorly defined. We analyzed plasma virus sequence evolution in 5.2-kb hemigenomes from multiple longitudinal time points isolated from individuals in the Irish anti-D cohort, who were infected with HCV from a common source in 1977 to 1978. We found phylogenetically distinct quasispecies populations at different plasma time points isolated late in chronic infection, suggesting ongoing viral evolution and quasispecies replacement over time. We saw evidence of early pressure driving net evolution away from a computationally reconstructed common ancestor, known as Bole1b, in predicted CTL epitopes and E1E2, with balanced evolution toward and away from the Bole1b amino acid sequence in the remainder of the genome. Late in chronic infection, the rate of evolution toward the Bole1b sequence increased, resulting in net neutral evolution relative to Bole1b across the entire 5.2-kb hemigenome. Surprisingly, even late in chronic infection, net amino acid evolution away from the infecting inoculum sequence still could be observed. These data suggest that, late in chronic infection, ongoing HCV evolution is not random genetic drift but rather the product of strong pressure toward a common ancestor and concurrent net ongoing evolution away from the inoculum virus sequence, likely balancing replicative fitness and ongoing immune escape.

Indexed as

Evolution, MolecularAmino Acid SequenceBase SequenceFemaleGenetic FitnessGenome, ViralHepacivirusHepatitis C, ChronicHumansImmune EvasionIrelandModels, GeneticMolecular Sequence DataPhylogenyReverse Transcriptase Polymerase Chain ReactionSequence Analysis, DNA

Identifiers

PMID22973048
PMCPMC3497661
OpenAlexW2115254140

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.