Genomic Evolution and Surveillance of Respiratory Syncytial Virus during the 2023

Genomic Evolution and Surveillance of Respiratory Syncytial Virus during the 2023–2024 Season

Published:2024-07-12 Issue:7 Volume:16 Page:1122
ISSN:1999-4915
Container-title:Viruses
language:en
Short-container-title:Viruses

Author:

Yunker Madeline¹^ORCID,Fall Amary¹,Norton Julie M.¹,Abdullah Omar¹,Villafuerte David A.¹^ORCID,Pekosz Andrew²³^ORCID,Klein Eili²⁴^ORCID,Mostafa Heba H.¹

Affiliation:

1. Johns Hopkins School of Medicine, Department of Pathology, Division of Medical Microbiology, Meyer B-121F, 600 N. Wolfe St., Baltimore, MD 21287, USA

2. Department of Emergency Medicine, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA

3. W. Harry Feinstone Department of Molecular Microbiology and Immunology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21287, USA

4. Center for Disease Dynamics, Economics, and Policy, Washington, DC 20005, USA

Abstract

Respiratory syncytial virus (RSV) is a significant cause of morbidity, particularly in infants. This study describes RSV genomic diversity and disease outcomes during the 2023–2024 season in the Johns Hopkins Hospital System (JHHS). Between August and December 2023, 406 patient samples were sequenced, showing that RSV-B GB5.0.5a was the dominant genotype detected. RSV-A genotype GA2.3.5 was detected less frequently. Metadata analysis of patient data revealed that, although RSV-B was more commonly detected, patients with RSV-A infections were more frequently hospitalized. Analysis of both the G- and F-genes revealed multiple amino acid substitutions in both RSV-A and RSV-B, with some positions within the F-protein that could be associated with evasion of antibody responses. Phylogenetic analysis revealed the genetic diversity of circulating GB5.0.5a and GA2.3.5 genotypes. This study serves as an important baseline for genomic surveillance of RSV within the JHHS and will assist in characterizing the impact of the newly approved RSV vaccines on RSV genomic evolution and the emergence of escape mutations.

Publisher

MDPI AG

Link

https://www.mdpi.com/1999-4915/16/7/1122/pdf

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