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Review
. 2024 Oct 9;33(174):240106.
doi: 10.1183/16000617.0106-2024. Print 2024 Oct.

Antibody-mediated protection against respiratory syncytial virus in children

Emma L Coindy  1 , Claudia Efstathiou  1 , Shubha Talwar  1 , Annick Moureau  2 , Charlotte Vernhes  2 , Peter J M Openshaw  1 , Ryan S Thwaites  3 ; PROMISE investigators
Affiliations
Review

Antibody-mediated protection against respiratory syncytial virus in children

Emma L Coindy et al. Eur Respir Rev. .

Abstract

Respiratory syncytial virus (RSV) is a major global pathogen, causing lower respiratory tract disease in at-risk populations including young children. Antibodies form a crucial layer of protection from RSV disease, particularly in immunologically naïve infants. Such antibodies are derived from the mother via transplacental transfer and breast milk, but may be particularly low in high-risk infants such as those born preterm. Maternally derived antibodies can now be supplemented by the administration of anti-RSV monoclonal antibodies, while a rising wave of maternal and paediatric vaccine strategies are approaching. The implementation of these prophylactics may profoundly decrease the healthcare burden of RSV. In this article, we review the role of antibody-mediated immunity in protecting children from RSV. We focus on maternally derived antibodies as the main source of protection against RSV and study factors that influence the scale of this transfer. The role of passive and active prophylactic approaches in protecting infants against RSV are discussed and knowledge gaps in our understanding of antibody-mediated protection against RSV are identified.

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Conflict of interest statement

Conflict of interest: A. Moureau is an employee of Sanofi and owns Sanofi stock as an employee. C. Vernhes was an employee of Sanofi at the time the work was performed, owns Sanofi stock as a former employee and is currently employed by the trade association Vaccines Europe. P.J.M. Openshaw reports consulting fees from GSK, Moderna, Janssen, Seqirus, Pfizer, Sanofi, AstraZeneca, and Icosavax; honoraria for lectures from GSK, Moderna, Seqirus, Sanofi, and AstraZeneca; participation on a Data Safety Monitoring Board for Sanofi; board membership for the Science Media Centre and a role as governor for Sidcot School. R.S. Thwaites reports consulting fees from AOBiome, Gossamer Bio, Indalo Therapeutics, and PrEP Biopharm; and honoraria for lectures from AstraZeneca and GSK. All other authors report no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Infant blood anti-respiratory syncytial virus (RSV) IgG and IgA titres. Maternally derived IgG is evident in the infant's blood from birth but declines rapidly to undetectable levels around 4 months of age. Following RSV infection, de novo antibody responses occur in infants older than 1–2 months of life, resulting in IgG and IgA titre rises. Created with Biorender.com.
FIGURE 2
FIGURE 2
Maternal antibody transfer in preterm, low- and high-titre scenarios. The scale of maternal antibody transfer profoundly influences the scale of antibody transfer to infants. In the scenario of preterm birth, transplacental antibody transfer may be low, resulting in low titres of anti-respiratory syncytial virus (RSV) antibodies in infants and high probability of susceptibility to severe RSV from birth. In maternal low-titre scenarios with term births, transplacental transfer does occur, but may quickly decay below a protective threshold. The amount of antibody needed to achieve this protective threshold is unknown and may be influenced by demographic and environmental factors. In high-titre scenarios, robust transplacental antibody transfer occurs, possibly owing to recent maternal RSV infection or vaccination. These high titres provide a longer window of protection against susceptibility to severe RSV infection. FcRN: neonatal Fc receptor. Created with Biorender.com.
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