• Asthma
• asthma epidemiology
• asthma genetics
• paediatric asthma
• respiratory infection
• viral infection

Patients with asthma and pregnancy were found as two groups most at risk for severe respiratory outcomes during the H1N1 epidemic in 2008.1–4 This association raises the question as to what immune dysfunctions may link these two conditions together and lead to an increased susceptibility for viral respiratory infections, and whether both patient populations may have similar defects in antiviral activity. This important and interesting clinical question is the focus of the paper by Forbes et al5 in Thorax.

In both asthma and pregnancy, there is a loss of the normal Th1/Th2 balance.6 7 In pregnancy, the shift away from a Th1 expression and towards a Th2 dominance during gestation likely reflects an ‘immune necessity’ to prevent the mother from having a ‘graft versus host’ reaction and subsequent loss of the pregnancy.7 In asthma, the immune picture is more complex, but the possible contribution of a Th1/Th2 imbalance with the presence of allergic reactions has been the basis of the hygiene hypothesis and target of new treatments.8 In broad-based terms, allergic sensitisation represents an overexpression of Th2 cytokines, interleukin (IL)-4, IL-5 and IL-13, with the resulting production of IgE antibodies with a capacity to cause allergic inflammation following allergen activation. In asthma, and pregnancy, a shift towards Th2 dominance also means a possible reduction in Th1 cytokines, such as interferons. The consequence of diminished interferon generation could explain the increased risk for respiratory infections in both asthma and pregnancy.

A deficiency in the generation of interferon has been most extensively studied in asthma and has been proposed as a risk factor …