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Severe respiratory syncytial virus disease in preterm infants: a case of innate immaturity
  1. Jeremy Anderson1,
  2. Lien Anh Ha Do1,2,
  3. Danielle Wurzel1,2,3,
  4. Zheng Quan Toh1,2,
  5. Kim Mulholland1,2,4,
  6. Daniel G Pellicci1,2,
  7. Paul V Licciardi1,2
  1. 1Infection and Immunity, Murdoch Children's Research Institute, Melbourne, Victoria, Australia
  2. 2Department of Pediatrics, The University of Melbourne—Parkville Campus, Melbourne, Victoria, Australia
  3. 3The Royal Children's Hospital Melbourne, Parkville, Victoria, Australia
  4. 4Epidemiology and Population Health, London School of Hygiene & Tropical Medicine, London, UK
  1. Correspondence to Professor Paul V Licciardi, Infection and Immunity, Murdoch Childrens Research Institute, Melbourne, VIC 3052, Australia; paul.licciardi{at}mcri.edu.au

Abstract

Respiratory syncytial virus (RSV) is the most common viral pathogen associated with acute lower respiratory tract infection (LRTI) in children under 5 years of age. Severe RSV disease is associated with the development of chronic respiratory complications such as recurrent wheezing and asthma. A common risk factor for developing severe RSV disease is premature gestation and this is largely due to an immature innate immune system. This increases susceptibility to RSV since the innate immune system is less able to protect against pathogens at a time when adaptive immunity has not fully developed. This review focuses on comparing different aspects of innate immunity between preterm and term infants to better understand why preterm infants are more susceptible to severe RSV disease. Identifying early life innate immune biomarkers associated with the development of severe RSV disease, and understanding how these compare between preterm and term infants, remains a critically important question that would aid the development of interventions to reduce the burden of disease in this vulnerable population.

  • respiratory infection
  • innate immunity

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Footnotes

  • Contributors PVL and JA conceived the idea for this manuscript. JA prepared the initial draft with contributions from LAHD, DW, KM, ZQT and DGP. All authors provided important intellectual input and critically revised the manuscript. All authors approved the final version of this manuscript to be submitted.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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