Abstract
A sudden increase in the rate of asthma exacerbations has been observed among young children in many countries 2-3 weeks after their return-to-school following the summer holidays. These exacerbations are frequently associated with human rhinovirus (hRV) infections, with possible interactions with allergen sensitisation, allergen exposure and medication use. It was originally proposed that the sudden increase resulted from new strains of respiratory viruses acquired during the holidays spreading rapidly on return to school. While there is compelling evidence implicating hRV in these exacerbations, recent observations on virus transmission, infection patterns and immune responses to both viruses and allergens have led us to propose an additional hypothesis for this increase in exacerbations. We propose that classrooms typically provide persistent exposure to a mixture of airborne viruses, viral proteins, endotoxin, community allergens and other human-derived aerosols - a modern miasma. During the preceding school term, this exposure establishes and maintains a level of immune tolerance and herd immunity, which then declines during the two-month holidays due to lack of such exposure, creating a transitory window of susceptibility to viral infections and asthma. The return to school re-establishes exposure to these aerosols resulting in an acceleration of exacerbations, until the tolerance and herd immunity are re-established. Thus, the peak in return-to-school asthma is more a function of a transitory increase in susceptibility due to a temporary lack of this complex exposure, than it is to novel, locally endemic strains of hRV.
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