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The immunology of virus infection in asthma

National Heart and Lung Institute, Dept of Respiratory Medicine, Imperial College School of Medicine at St Mary's, London, UK

CORRESPONDENCE: S.D. Message, National Heart and Lung Institute, Dept of Respiratory Medicine, Imperial College School of Medicine at St Mary's, Norfolk Place, London, W2 1PG, UK. Fax: 44 2072628913

Keywords: asthma, immune response, respiratory virus infections

Received: March 22, 2001
Accepted May 8, 2001

This work was supported by the Medical Research Council and the British Lung Foundation.

Abstract

The respiratory tract is commonly infected by a range of viruses with overlapping pathologies. The majority of episodic exacerbations of asthma are associated with viral infection, in particular with rhinovirus infections.

Experimental rhinovirus infection in human volunteers provides a useful model of natural virus-induced asthma. The asthmatic airway is characterized by an infiltrate of eosinophils and T-lymphocytes expressing the type 2 cytokines interleukin (IL)-4, IL-5 and IL-13. An effective antiviral immune response requires early viral clearance and appropriate termination of the immune response to minimize associated immunopathology and tissue damage.

The antiviral immune response is made up of innate (nonspecific) and specific components, and requires the coordinated actions of many different cell types including neutrophils, macrophages, eosinophils, dendritic cells, epithelial cells, mast cells, natural killer cells and B- and T-lymphocytes. Coordination of this response involves numerous cytokines and chemokines. T-lymphocytes expressing type 1 cytokines including interferon- play a key role.

Pre-existing asthmatic inflammation in the lower airway may modify the immune response to viral infection by altering the balance of T-cell cytokine expression from type 1 towards a type 2 in what is always a mixed response. The consequence is delayed viral clearance, persistent virus-induced inflammation and amplification of the allergic inflammation.

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