Respiratory syncytial virus bronchiolitis and the pathogenesis of childhood asthma

Pediatr Infect Dis J. 2003 Feb;22(2 Suppl):S76-82. doi: 10.1097/01.inf.0000053889.39392.a7.

Abstract

There is now convincing evidence that children who develop lower respiratory symptoms during infection with respiratory syncytial virus (RSV) in early life are at increased risk of developing asthma-like symptoms during the school years. What determines this association is not well-understood, but increased likelihood of allergic sensitization plays a minor role, if any, as a determinant of post-RSV wheeze. Current evidence suggests that both genetic and environmental factors determine the type of immune response to the acute RSV infection and that this response, in turn, may affect the development of the control mechanisms involved in the regulation of airway tone. Many different cytokines appear to play a role in this acute immune response, including interferon-gamma; interleukins 8, 10 and 12; and cytokines produced by T helper (Th) 1 and Th2 cells. Because asthma is a heterogeneous condition, future studies will need to determine the potentially different role of RSV infection as a risk factor for these different asthma phenotypes. It is likely, however, that strategies for the prevention of RSV infection may play a role in the prevention of the subsequent development of persistent wheezing and asthma-like symptoms in childhood.

Publication types

  • Review

MeSH terms

  • Asthma / etiology*
  • Asthma / virology*
  • Bronchiolitis, Viral / complications*
  • Child
  • Child, Preschool
  • Cytokines / immunology
  • Genetic Predisposition to Disease
  • Humans
  • Immunity, Cellular
  • Immunization
  • Infant
  • Infant, Newborn
  • Lung / physiology
  • Phenotype
  • Respiratory Sounds / etiology
  • Respiratory Sounds / immunology
  • Respiratory Syncytial Virus Infections / complications*
  • Respiratory Syncytial Virus Infections / genetics
  • Respiratory Syncytial Virus Infections / pathology
  • Respiratory Syncytial Virus, Human / pathogenicity*
  • Risk Factors

Substances

  • Cytokines