Viruses and asthma

Asthma is a chronic inflammatory airway disease with two essential components: bronchial inflammation and airway remodelling. The pathophysiologic patterns arise from an intricate network of interactions between genetic and environmental factors, including mainly respiratory viruses.

Epidemiologic association between viral bronchiolitis in infancy, mainly RSV bronchiolitis, and asthma development later in life has been described for decades. The different children response after RSV infection might depend on genetic factors related with Th1/Th2 immunologic balance. Furthermore, several genetic polymorphisms have been associated with changes in cytokines, IgE levels and higher frequency of wheezing episodes. In the other hand, recent studies have shown that other viruses as rhinovirus and human metapneumovirus might impose an even higher risk or asthma than RSV. However, other studies have shown that some infections, especially those occurred early in life, might protect for asthma development.

An association between colds and asthma exacerbations has long been recognized, but early studies yielded low virus detection rates of approximately 10%-25%. Recently the use of polymerase chain reaction (PCR)-based methods, has shown that respiratory viruses are responsible for a much higher proportion of asthma exacerbations. RSV and rhinovirus are by far the most frequent. The exact molecular mechanisms by which viruses cause exacerbations in predisposed subjects remain unclear. However, several inflammatory mediators, mainly IL-6, IL-8, IL-11 and IL-16, that lead to an influx of inflammatory cells into the airway, have been implicated. The release of inflammatory cell products (eosinophil cationic protein, elastase, etc) might also contribute to the pathophysiology of asthmatic obstruction.