Respiratory viral infections in children with asthma: do they matter and can we prevent them?

While the importance of preventing viral infection is well established, preventive strategies have not been well explored. Good personal hygiene, hand-washing and avoidance of cigarette smoke are likely to reduce respiratory viral infections. Eating a healthy balanced diet, active probiotic supplements and bacterial-derived products, such as OM-85, may reduce recurrent infections in susceptible children. There are no practical anti-viral therapies currently available that are suitable for widespread use.Hand hygiene is the best measure to prevent the common cold. A healthy balanced diet, active probiotic supplements and immunostimulant OM-85 may reduce recurrent infections in asthmatic children.Asthma is a major public health problem with a huge social and economic burden affecting 300 million people worldwide [1]. Viral respiratory infections are the major cause of acute asthma exacerbations and contribute to asthma inception in high risk young children with susceptible genetic background. A history of wheeze associated with respiratory viral infections early in life is one of the major risk factors for the later development of asthma [2-7], together with sensitization to aeroallergens in early life and a family history of asthma and allergies, reflecting a genetic predisposition. Respiratory viral infections are also the principal cause of asthma exacerbations in children and adults [8-13]. However, the question of whether viral infections “select” susceptible hosts or whether viral infections may induce asthma de novo by “damaging” airways is not settled. In other words, do viruses cause or simply unmask asthma?Respiratory viruses first infect nasal epithelial cells which triggers an antiviral response. This response is driven by type I (α/β) and III (λ) interferons (IFN) that are induced following recognition of viral ribonucleic acid (RNA) by pattern recognition receptors (PRRs). Toll-like receptors (TLRs) are cell surface and endosomal PRRs, whilst the RNA hel