Viral infections are responsible for the majority of asthma attacks in both children and adults. Vagally mediated reflex bronchoconstriction is potentiated due to loss of function of inhibitory M2 muscarinic receptors on the airway parasympathetic nerves. Multiple mechanisms are involved. Production of interferons may down regulate the expression of the M2 receptor gene. This effect is reversed by steroids. In allergic animals (and perhaps in atopic humans) eosinophils are recruited to the airway nerves, where they are activated, releasing major basic protein, which binds to the M2 receptors, blocking their function. Despite these negative physiological consequences of eosinophil activation, eosinophils are capable of exerting a potent antiviral effect. Thus, the inflammatory response to viral infections may have positive, as well as negative, consequences.