Infantile respiratory syncytial virus and human rhinovirus infections: respective role in inception and persistence of wheezing

Eur Respir J. 2015 Mar;45(3):774-89. doi: 10.1183/09031936.00062714. Epub 2014 Oct 30.

Abstract

There is evidence that respiratory viruses play a key role in the development and exacerbation of obstructive respiratory diseases in children. This review attempts to juxtapose the separate profiles and prototypes of pathogenetic mechanisms represented by the two most common amongst such viruses: respiratory syncytial virus (RSV) and human rhinovirus (HRV). RSV represents the most common agent of severe airway disease in infants and young children, and is predominant in winter months. Large epidemiological studies have revealed an unequivocal relationship between RSV infection and subsequent wheezing into childhood, thought to be related to long-term changes in neuroimmune control of the airways rather than allergic sensitisation. HRV is a highly diverse group of viruses that affect subjects of all ages, is ubiquitous and occurs year-round. In contrast to RSV, infections with HRV cause minimal cytotoxicity but induce a rapid production of cytokines and chemokines with amplification of the inflammatory response. The susceptibility to HRV-induced bronchiolitis and subsequent wheezing appears to be linked to individual predisposition since it is often associated with a family or personal history of asthma/atopy. Thus, RSV probably serves as an "inducer" rather than a "trigger". Conversely, HRVs seem to serve as a "trigger" rather than an "inducer" in predisposed individuals.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Host-Pathogen Interactions / immunology
  • Humans
  • Infant
  • Picornaviridae Infections* / immunology
  • Picornaviridae Infections* / physiopathology
  • Respiratory Sounds / physiopathology
  • Respiratory Syncytial Virus Infections* / immunology
  • Respiratory Syncytial Virus Infections* / physiopathology
  • Respiratory Syncytial Virus, Human / pathogenicity*
  • Rhinovirus / pathogenicity*