Genomic characterization of hepatitis C virus transmitted founder variants with deep sequencing.


Journal

Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases
ISSN: 1567-7257
Titre abrégé: Infect Genet Evol
Pays: Netherlands
ID NLM: 101084138

Informations de publication

Date de publication:
07 2019
Historique:
received: 02 12 2018
revised: 26 02 2019
accepted: 28 02 2019
pubmed: 12 3 2019
medline: 11 2 2020
entrez: 12 3 2019
Statut: ppublish

Résumé

Transfer of hepatitis C virus (HCV) infection from a donor to a new recipient is associated with a bottleneck of genetic diversity in the transmitted viral variants. Existing data suggests that one, or very few, variants emerge from this bottleneck to establish the infection (transmitted founder [T/F] variants). In HCV, very few T/F variants have been characterized due to the challenges of obtaining early infection samples and of high throughput viral genome sequencing. This study used a large, acute HCV, deep-sequenced dataset from first viremia samples collected in nine prospective cohorts across four countries, to estimate the prevalence of single T/F viruses, and to identify host and virus-related factors associated with infections initiated by a single T/F variant. The short reads generated by Illumina sequencing were used to reconstruct viral haplotypes with two haplotype reconstruction algorithms. The haplotypes were examined for random mutations (Poisson distribution) and a star-like phylogeny to identify T/F viruses. The findings were cross-validated by haplotype reconstructions across three regions of the genome (Core-E2, NS3, NS5A) to minimize the possibility of spurious overestimation of single T/F variants. Of 190 acute infection samples examined, 54 were very early acute infections (HCV antibody negative, RNA positive), and single transmitted founders were identified in 14 (26%, 95% CI: 16-39%) after cross validation across multiple regions of the genome with two haplotype reconstruction algorithms. The presence of a single T/F virus was not associated with any host or virus-related factors, notably viral genotype or spontaneous clearance. In conclusion, approximately one in four new HCV infections originates from a single T/F virus. Resolution of genomic sequences of single T/F variants is the first step in exploring unique properties of these variants in the infection of host hepatocytes.

Identifiants

pubmed: 30853512
pii: S1567-1348(18)30936-5
doi: 10.1016/j.meegid.2019.02.032
pmc: PMC6487228
mid: NIHMS1524442
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

36-41

Subventions

Organisme : NIDA NIH HHS
ID : R01 DA015999
Pays : United States
Organisme : NIDA NIH HHS
ID : R01 DA031056
Pays : United States
Organisme : NIDA NIH HHS
ID : R01 DA016017
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI066345
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI105035
Pays : United States
Organisme : NIAID NIH HHS
ID : U01 AI131314
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI088791
Pays : United States
Organisme : CIHR
ID : MOP-103138
Pays : Canada
Organisme : CIHR
ID : MOP-106468
Pays : Canada

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

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Auteurs

Arunasingam Abayasingam (A)

School of Medical Sciences, Faculty of Medicine, UNSW, Sydney, NSW, Australia.

Preston Leung (P)

The Kirby Institute, UNSW, Sydney, NSW, Australia.

Auda Eltahla (A)

School of Medical Sciences, Faculty of Medicine, UNSW, Sydney, NSW, Australia.

Rowena A Bull (RA)

School of Medical Sciences, Faculty of Medicine, UNSW, Sydney, NSW, Australia.

Fabio Luciani (F)

School of Medical Sciences, Faculty of Medicine, UNSW, Sydney, NSW, Australia.

Jason Grebely (J)

The Kirby Institute, UNSW, Sydney, NSW, Australia.

Gregory J Dore (GJ)

The Kirby Institute, UNSW, Sydney, NSW, Australia.

Tanya Applegate (T)

The Kirby Institute, UNSW, Sydney, NSW, Australia.

Kimberly Page (K)

Division of Epidemiology, Biostatistics and Preventive Medicine, University of New Mexico, Albuquerque, NM, USA.

Julie Bruneau (J)

CRCHUM, Université de Montréal, Montreal, QC, Canada.

Andrea L Cox (AL)

Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD, USA.

Arthur Y Kim (AY)

Harvard Medical School, Boston, MA, USA.

Janke Schinkel (J)

Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine and AIDS, Center for Infection and Immunity Amsterdam, Academic Medical Center, Meibergdreef 9, Amsterdam, The Netherlands.

Naglaa H Shoukry (NH)

CRCHUM, Université de Montréal, Montreal, QC, Canada.

Georg M Lauer (GM)

Harvard Medical School, Boston, MA, USA.

Lisa Maher (L)

The Kirby Institute, UNSW, Sydney, NSW, Australia.

Margaret Hellard (M)

Burnet Institute, Melbourne, VIC, Australia; Monash University, Melbourne, Australia; Alfred Hospital, Melbourne, Australia; Doherty Institute and Melbourne School of Population and Global Health, University of Melbourne, Australia.

Maria Prins (M)

Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine and AIDS, Center for Infection and Immunity Amsterdam, Academic Medical Center, Meibergdreef 9, Amsterdam, The Netherlands; GGD Public Health Service of Amsterdam, Amsterdam, The Netherlands.

Andrew Lloyd (A)

The Kirby Institute, UNSW, Sydney, NSW, Australia.

Chaturaka Rodrigo (C)

School of Medical Sciences, Faculty of Medicine, UNSW, Sydney, NSW, Australia. Electronic address: c.rodrigo@unsw.edu.au.

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Classifications MeSH