Author
Listed:
- Gu-Lung Lin
(University of Oxford
NIHR Oxford Biomedical Research Centre)
- Simon B. Drysdale
(University of Oxford
NIHR Oxford Biomedical Research Centre
University of London)
- Matthew D. Snape
(University of Oxford
NIHR Oxford Biomedical Research Centre)
- Daniel O’Connor
(University of Oxford
NIHR Oxford Biomedical Research Centre)
- Anthony Brown
(University of Oxford)
- George MacIntyre-Cockett
(University of Oxford)
- Esther Mellado-Gomez
(University of Oxford)
- Mariateresa Cesare
(University of Oxford)
- David Bonsall
(University of Oxford
University of Oxford)
- M. Azim Ansari
(University of Oxford)
- Deniz Öner
(Janssen Pharmaceutica NV)
- Jeroen Aerssens
(Janssen Pharmaceutica NV)
- Christopher Butler
(University of Oxford)
- Louis Bont
(University Medical Center Utrecht
ReSViNET Foundation)
- Peter Openshaw
(Imperial College London)
- Federico Martinón-Torres
(Hospital Clínico Universitario de Santiago de Compostela
Instituto de Investigación Sanitaria de Santiago de Compostela)
- Harish Nair
(University of Edinburgh)
- Rory Bowden
(University of Oxford
Walter and Eliza Hall Institute of Medical Research)
- Tanya Golubchik
(University of Oxford)
- Andrew J. Pollard
(University of Oxford
NIHR Oxford Biomedical Research Centre)
Abstract
Human respiratory syncytial virus (RSV) is a major cause of lower respiratory tract infection in young children globally, but little is known about within-host RSV diversity. Here, we characterised within-host RSV populations using deep-sequencing data from 319 nasopharyngeal swabs collected during 2017–2020. RSV-B had lower consensus diversity than RSV-A at the population level, while exhibiting greater within-host diversity. Two RSV-B consensus sequences had an amino acid alteration (K68N) in the fusion (F) protein, which has been associated with reduced susceptibility to nirsevimab (MEDI8897), a novel RSV monoclonal antibody under development. In addition, several minor variants were identified in the antigenic sites of the F protein, one of which may confer resistance to palivizumab, the only licensed RSV monoclonal antibody. The differences in within-host virus populations emphasise the importance of monitoring for vaccine efficacy and may help to explain the different prevalences of monoclonal antibody-escape mutants between the two subgroups.
Suggested Citation
Gu-Lung Lin & Simon B. Drysdale & Matthew D. Snape & Daniel O’Connor & Anthony Brown & George MacIntyre-Cockett & Esther Mellado-Gomez & Mariateresa Cesare & David Bonsall & M. Azim Ansari & Deniz Öne, 2021.
"Distinct patterns of within-host virus populations between two subgroups of human respiratory syncytial virus,"
Nature Communications, Nature, vol. 12(1), pages 1-11, December.
Handle:
RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-25265-4
DOI: 10.1038/s41467-021-25265-4
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Citations
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Cited by:
- Deshan Perera & Evan Li & Paul MK Gordon & Frank Meer & Tarah Lynch & John Gill & Deirdre L. Church & A. P. Jason Koning & Christian D. Huber & Guido Marle & Alexander Platt & Quan Long, 2025.
"Apollo: a comprehensive GPU-powered within-host simulator for viral evolution and infection dynamics across population, tissue, and cell,"
Nature Communications, Nature, vol. 16(1), pages 1-17, December.
- Gu-Lung Lin & Simon B. Drysdale & Matthew D. Snape & Daniel O’Connor & Anthony Brown & George MacIntyre-Cockett & Esther Mellado-Gomez & Mariateresa Cesare & M. Azim Ansari & David Bonsall & James E. , 2024.
"Targeted metagenomics reveals association between severity and pathogen co-detection in infants with respiratory syncytial virus,"
Nature Communications, Nature, vol. 15(1), pages 1-14, December.
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