Spatial and temporal transmission dynamics of respiratory syncytial virus in New Zealand before and after the COVID-19 pandemic

期刊论文
出版模式：

开放获取
发表日期：

2024年11月11日

查看全文

Lauren Jelley,
Jordan Douglas,
Meaghan O’Neill,
Klarysse Berquist,
Ana Claasen,
Jing Wang,
Srushti Utekar,
Helen Johnston,
Judy Bocacao,
Margot Allais,
Joep de Ligt,
Chor Ee Tan,
Ruth Seeds,
Tim Wood,
Nayyereh Aminisani,
Tineke Jennings,
David Welch,
Nikki Turner,
Peter McIntyre,
Tony Dowell,
Adrian Trenholme,
Cass Byrnes,
Bryden Bird,
Tegan Slater,
Farjana Ahmed,
Mai Anh Sam,
Elaisa Glampe,
Gabriella Davey,
Mary Ryan,
Megan Rensburg,
Jort Cueto,
Ernest Caballero,
Joshma John,
Sasha Aizupuru,
Maritza Marull,
Andrea Bowers,
Paul Thomas,
Richard Webby,
Nigel French,
Q. Sue Huang,
David Winter,
Jemma L. Geoghegan

摘要

Human respiratory syncytial virus (RSV) is a major cause of acute respiratory infection. In 2020, RSV was eliminated from New Zealand due to non-pharmaceutical interventions (NPI) used to control the spread of SARS-CoV-2. However, in 2021, following a brief quarantine-free travel agreement with Australia, there was a large-scale nationwide outbreak of RSV that led to reported cases more than five-times higher than typical seasonal patterns. We generated 1470 viral genomes of both RSV-A and RSV-B sampled between 2015–2022 from across New Zealand. Using a phylodynamics approach, we used these data to better understand RSV transmission patterns in New Zealand prior to 2020, and how RSV became re-established in the community following the relaxation of COVID-19 restrictions. We found that in 2021, there was a large epidemic of RSV due to an increase in importations, leading to several large genomic clusters of both RSV-A ON1 and RSV-B BA9 genotypes. However, while a number of viral importations were detected, there was also a major reduction in RSV genetic diversity compared to pre-pandemic years. These data reveal the impact of NPI used during the COVID-19 pandemic on other respiratory infections and highlight the important insights that can be gained from viral genomes.