Reply

We thank Tam and Grayson1 for their correspondence and for raising the interesting possibility that rhinovirus-specific IgE might play a role in mediating the severity of rhinovirus-triggered asthma exacerbation. Although our data do not exclude this possibility, we point out several lines of evidence that support the key role that allergic sensitization (mainly to house dust mite) plays in influencing the clinical phenotype of rhinovirus infection: (1) There is a robust interaction between early life sensitization to dust mite and early life rhinovirus infection that amplifies the risk of asthma inception later in life.

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