Evidence map›Paper›PMID 30602023›Full record

ArticleThe Journal of infectious diseases2019

High-Resolution Evolutionary Analysis of Within-Host Hepatitis C Virus Infection.

Jayna Raghwani, Chieh-Hsi Wu, Cynthia K Y Ho, Menno De Jong, Richard Molenkamp, Janke Schinkel, Oliver G Pybus, Katrina A Lythgoe

Abstract read
In one paragraph

Article in The Journal of infectious diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
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  11. Inconsistent temporal patterns of genetic variation of HCV among high-risk subjects may impact inference of transmission networks.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2019
    Article
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

8 authors.

Jayna RaghwaniBig Data Institute, Li Ka Shing Centre for Health Information and Discovery, Nuffield Department of Medicine, University of Oxford, United Kingdom.
Chieh-Hsi WuDepartment of Statistics, University of Oxford, United Kingdom.
Cynthia K Y HoDepartment of Medical Microbiology, Amsterdam University Medical Center, the Netherlands.
Menno De JongDepartment of Medical Microbiology, Amsterdam University Medical Center, the Netherlands.
Richard MolenkampDepartment of Medical Microbiology, Amsterdam University Medical Center, the Netherlands.
Janke SchinkelDepartment of Medical Microbiology, Amsterdam University Medical Center, the Netherlands.
Oliver G PybusDepartment of Zoology, University of Oxford, United Kingdom.
Katrina A LythgoeBig Data Institute, Li Ka Shing Centre for Health Information and Discovery, Nuffield Department of Medicine, University of Oxford, United Kingdom.

Funding

European Research Council 614725Wellcome Trust 107652
6 · The paper itself

Abstract

backgroundDespite recent breakthroughs in treatment of hepatitis C virus (HCV) infection, we have limited understanding of how virus diversity generated within individuals impacts the evolution and spread of HCV variants at the population scale. Addressing this gap is important for identifying the main sources of disease transmission and evaluating the risk of drug-resistance mutations emerging and disseminating in a population.

methodsWe have undertaken a high-resolution analysis of HCV within-host evolution from 4 individuals coinfected with human immunodeficiency virus 1 (HIV-1). We used long-read, deep-sequenced data of full-length HCV envelope glycoprotein, longitudinally sampled from acute to chronic HCV infection to investigate the underlying viral population and evolutionary dynamics.

resultsWe found statistical support for population structure maintaining the within-host HCV genetic diversity in 3 out of 4 individuals. We also report the first population genetic estimate of the within-host recombination rate for HCV (0.28 × 10-7 recombination/site/year), which is considerably lower than that estimated for HIV-1 and the overall nucleotide substitution rate estimated during HCV infection.

conclusionsOur findings indicate that population structure and strong genetic linkage shapes within-host HCV evolutionary dynamics. These results will guide the future investigation of potential HCV drug resistance adaptation during infection, and at the population scale.

Indexed as

Evolution, MolecularGenetic VariationAntiviral AgentsCoinfectionDrug Resistance, ViralGenetics, PopulationGenotypeHepacivirusHepatitis CHepatitis C, ChronicHigh-Throughput Nucleotide SequencingHIV-1HIV InfectionsHumansMolecular EpidemiologyRecombination, GeneticAntiviral Agentshepatitis C virusmolecular epidemiologyphylogeneticspopulation geneticsrecombinationviral evolutionviral replication

Identifiers

PMID30602023
PMCPMC6500553

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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.