Childhood viral infection and the pathogenesis of asthma and chronic obstructive lung disease

Am J Respir Crit Care Med. 1999 Nov;160(5 Pt 2):S26-8. doi: 10.1164/ajrccm.160.5.8.

Abstract

Many epidemiologic studies have implicated childhood respiratory infections as an independent risk factor for the subsequent development of persistent asthma and chronic obstructive pulmonary disease (COPD). The majority of these childhood infections are viral in origin, and great strides are being made in understanding their pathogenesis at the molecular level. Some viruses, such as respiratory syncytial virus-a common cause of childhood bronchiolitis-stimulate the helper T cell type 2 (Th2) pattern of immune responses associated with allergic inflammation. Other viruses, such as adenovirus, appear to persist as latent infections in the airways of patients with COPD, and adenoviral E1A protein is capable of amplifying host genes, possibly including those involved in cigarette smoke-induced lung inflammation. Studies of the chronic, low-grade peripheral lung inflammation caused by adenoviral infection of guinea pigs will enable examination of the possibility that latent infection may induce resistance to the antiinflammatory actions of corticosteroids. Studies of the molecular mechanisms of viral infections of the airways could provide important insights into the nature of the inflammatory process involved in asthma and COPD. Hogg JC. Childhood viral infection and the pathogenesis of asthma and chronic obstructive lung disease.

Publication types

  • Review

MeSH terms

  • Adenovirus E1A Proteins / immunology
  • Adenovirus Infections, Human / immunology*
  • Adenoviruses, Human / immunology
  • Adult
  • Animals
  • Asthma / immunology
  • Bronchiolitis / immunology
  • Child
  • Guinea Pigs
  • Humans
  • Lung Diseases, Obstructive / immunology*
  • Respiratory Syncytial Virus Infections / immunology*
  • Respiratory Syncytial Virus, Human / immunology
  • Respiratory Tract Infections / immunology*
  • Smoking / adverse effects
  • Th2 Cells / immunology

Substances

  • Adenovirus E1A Proteins