Virus/Allergen Interaction in Asthma Exacerbation

Abstract

Allergy and viral respiratory infections have long been recognized as two of the most important risk factors for exacerbations of asthma. These observations have raised questions regarding potential interactions between these two important risk factors. For example, does allergy diminish the antiviral response, thereby promoting exacerbations of asthma? Alternately, do viral respiratory infections potentiate ongoing allergic inflammation in the airway? The answers to these questions are likely to have implications regarding the prevention and treatment of exacerbations of asthma. This article reviews that clinical evidence linking viral infections and allergy to exacerbations of asthma, reviews potential interactions between these two risk factors, and discusses possible application of new insights in virus/allergen interactions to the prevention and treatment of exacerbations of asthma.

Keywords: allergy; asthma; interferon; rhinovirus.

Figure 1.

High-affinity IgE receptors (FcεRIs) on plasmacytoid dendritic cells and effects on interferon responses. In the absence of allergy, plasmacytoid dendritic cells (pDCs) express low levels of cell surface FcεRI, and some of these receptors are occupied by IgE. Rhinovirus (RV) infection induces pDCs to secrete IFN-α and IFN-λ, which inhibit viral replication in an autologous and paracrine fashion. In the context of allergy with allergen exposure, FcεRI and IgE are increased, and cross-linking of receptors by allergen can inhibit interferon secretion. The net result in asthma could be increased viral replication, more severe illness, and increased risk for exacerbation of chronic asthma. Figure courtesy of William W. Busse, M.D., University of Wisconsin-Madison.