Our results are consistent with these previous researches because children with more severe clinical and radiological manifestations of H1N1 disease severity, such as ARDS and longer and dry cough, elicited a more intensive production of IL-1β and IL-6 than H1N1 mild patients, suggesting that this up-regulation exerted a key role in biochemical and molecular processes affecting the lung soon after the infection leading to the development of airway inflammation and bronchial hyperreactivity [29, 30]. The gene discussed is IL1B; the disease is acute respiratory distress syndrome.