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Updated: May 3, 2026

Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses
Published on: April 4, 2019
Genetic predisposition of RSV infection-related respiratory morbidity in preterm infants
Simon B Drysdale1, Michael Prendergast, Mireia Alcazar
1Division of Asthma, Allergy and Lung Biology, MRC-Asthma UK Centre in Allergic Mechanisms of Asthma, King's College London, London, UK.
Insights
Premature infants may have a genetic predisposition to respiratory syncytial virus (RSV) lower respiratory tract infections (LRTIs). Certain gene variations are linked to increased RSV LRTIs and long-term respiratory issues in these vulnerable infants.
Area of Science:
- Genetics
- Neonatology
- Pulmonology
Background:
- Premature infants are susceptible to respiratory syncytial virus (RSV) infections.
- RSV infection can lead to significant respiratory morbidity in preterm infants.
- The genetic basis for this susceptibility and subsequent morbidity is not fully understood.
Purpose of the Study:
- To investigate if genetic factors predispose prematurely born infants to respiratory morbidity from RSV infections.
- To identify specific genetic variations (SNPs) associated with RSV lower respiratory tract infections (LRTIs) and chronic respiratory outcomes.
Main Methods:
- Prospective follow-up of 146 infants born before 36 weeks gestation.
- Collection of nasopharyngeal aspirates during lower respiratory tract infections (LRTI).
- Genetic testing for 11 single-nucleotide polymorphisms (SNPs) and assessment of respiratory health and lung function.
Main Results:
- A specific single-nucleotide polymorphism (SNP) in the ADAM33 gene was associated with an increased risk of developing RSV LRTIs.
- SNPs in IL10, NOS2A, SFTPC, MMP16, and VDR genes were linked to increased chronic respiratory morbidity.
- Reduced lung function at 1 year was associated with SNPs in MMP16, NOS2A, SFTPC, and VDR in infants with prior RSV LRTIs.
Conclusions:
- Prematurely born infants may possess a genetic predisposition to RSV LRTIs.
- This genetic predisposition contributes to subsequent respiratory morbidity, independent of initial lung function.
- Specific gene variations play a role in both the susceptibility to RSV LRTIs and the development of chronic respiratory issues.
Unlabelled:
The aim of this study was to assess whether prematurely born infants have a genetic predisposition to respiratory syncytial virus (RSV) infection-related respiratory morbidity. One hundred and forty-six infants born at less than 36 weeks of gestation were prospectively followed. Nasopharygeal aspirates were obtained on every occasion the infants had a lower respiratory tract infection (LRTI) regardless of need for admission. DNA was tested for 11 single-nucleotide polymorphisms (SNPs). Chronic respiratory morbidity was assessed using respiratory health-related questionnaires, parent-completed diary cards at a corrected age of 1 year and review of hospital notes. Lung function was measured at a post menstrual age (PMA) of 36 weeks and corrected age of 1 year. A SNP in ADAM33 was associated with an increased risk of developing RSV LRTIs, but not with significant differences in 36-week PMA lung function results. SNPs in several genes were associated with increased chronic respiratory morbidity (interleukin 10 (IL10), nitric oxide synthase 2A (NOS2A), surfactant protein C (SFTPC), matrix metalloproteinase 16 (MMP16) and vitamin D receptor (VDR)) and reduced lung function at 1 year (MMP16, NOS2A, SFTPC and VDR) in infants who had had RSV LRTIs.
Conclusions:
Our results suggest that prematurely born infants may have a genetic predisposition to RSV LRTIs and subsequent respiratory morbidity which is independent of premorbid lung function.
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