A large effective population size for established within-host influenza virus infection

Abstract
Data availability
Article and author information
Metrics

Abstract

Strains of the influenza virus form coherent global populations, yet exist at the level of single infections in individual hosts. The relationship between these scales is a critical topic for understanding viral evolution. Here we investigate the within-host relationship between selection and the stochastic effects of genetic drift, estimating an effective population size of infection N_e for influenza infection. Examining whole-genome sequence data describing a chronic case of influenza B in a severely immunocompromised child we infer an N_e of 2.5 x 10⁷ (95% confidence range 1.0 x 10⁷ to 9.0 x 10⁷) suggesting that genetic drift is of minimal importance during an established influenza infection. Our result, supported by data from influenza A infection, suggests that positive selection during within-host infection is primarily limited by the typically short period of infection. Atypically long infections may have a disproportionate influence upon global patterns of viral evolution.

Data availability

All sequence data is taken from previous publications, and is available from the Sequence Read Archive. Where this is sensible, raw data underlying figures has been made available in files which accompany this document.

The following previously published data sets were used

1. Lumby K
2. Zhao L
3. Oporto M
4. Best T
5. Tutill H
6. Shah D
7. Veys P
8. Williams R
9. Worth A
10. Illingworth CJR
11. Breuer J
(2020) Favipiravir and zanamivir cleared infection with influenza B in a severely immunocompromised child
SRA BioProject, PRJNA601176.

https://doi.org/10.1093/cid/ciaa023
1. Xue KS
2. Stevens-Ayers T
3. Campbell AP
4. Englund JA
5. Pergam SA
6. Boeckh M
7. Bloom JD
(2017) Parallel evolution of influenza across multiple spatiotemporal scales
SRA BioProject, PRJNA364676.

http://doi.org/10.7554/eLife.26875

Article and author information

Author details

Casper K Lumby

Department of Genetics, University of Cambridge, Cambridge, United Kingdom

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0001-8329-9228
Lei Zhao

Department of Genetics, University of Cambridge, Cambridge, United Kingdom

Competing interests
The authors declare that no competing interests exist.
Judith Breuer

Division of Infection and Immunity, University College London, London, United Kingdom

Competing interests
The authors declare that no competing interests exist.
Christopher J R Illingworth

Department of Genetics, University of Cambridge, Cambridge, United Kingdom

For correspondence
cjri2@cam.ac.uk

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0002-0030-2784

Funding

Wellcome (101239/Z/13/Z)

Christopher J R Illingworth

Wellcome (101239/Z/13/A)

Christopher J R Illingworth

Wellcome (105365/Z/14/Z)

Casper K Lumby

Isaac Newton Trust

Christopher J R Illingworth

Helsingin Yliopisto

Christopher J R Illingworth

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Copyright

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.