Respiratory viruses in the development of allergy.

Citation
J. Brouard et al., Respiratory viruses in the development of allergy., ARCH PED, 6, 1999, pp. 29S-34S
Citations number
33
Categorie Soggetti
Pediatrics
Journal title
ARCHIVES DE PEDIATRIE
ISSN journal
0929693X → ACNP
Volume
6
Year of publication
1999
Supplement
1
Pages
29S - 34S
Database
ISI
SICI code
0929-693X(1999)6:<29S:RVITDO>2.0.ZU;2-7
Abstract
Viral respiratory tract infections are a major cause of wheezing in infants . Investigators determined that 80% to 85% of school-aged children with whe ezing episodes were tested positive for vints. To more fully understand how viral respiratory tract infections influence asthma, investigators have ev aluated the effect of respiratory tract infections on airway symptoms, func tion, and inflammation. Although the mechanisms by which respiratory viruse s enhance lower airway inflammation are not established cytokines may play a key role in this process. The respiratory epithelial cell is a principal host for respiratory virus replication and is likely to be the first source of cytokines during an acute infection. T cells orchestrate immune respons es to both allergens and viruses, and regulate effector cells with virucida l and proinflammatory effects. Although studies demonstrate that virus-spec ific T cells may contribute to virus-induced lung disease, evidence to defi ne the role of virus-specific T lymphocytes in asthma has nor been fully es tablished Some infections early in life may also have an important immunore gularly role in the subsequent development of allergy and asthma. Atopy is characterised by exaggerated Th-2 cell responses to common allergens with s ecretion of cytokines such as IL-4 and IL-5 that promote IgE production and eosinophil activation. In contrast, childhood infections typically induce a Th-l cell response, characterised by secretion of interferon-gamma, which enhances the antiviral activities of effector cells. These two types of T cell responses are mutually antagonistic. (C) 1999 Elsevier, Paris.