However, the decline in lung function that is associated with development of chronic infection with P. aeruginosa is not constant or linear. Instead, periods of relatively stable lung function are interrupted by episodes with an acute drop in lung function, from which full recovery might not be achieved by antibiotic treatment (10). Causes and pathological mechanisms involved in these pulmonary exacerbations are often unclear and bacterial and viral infections have been attributed to it (11). Virus-induced pulmonary exacerbations are well-known in other lung diseases like COPD or asthma (12). Yet, the importance of viral induced pulmonary exacerbations in CF patients is still unclear (13, 14). However, it has been shown that the lung microbiome composition itself is quite resilient and does not change to great extent in most cases of exacerbation (15, 16) and therefore the involvement of non-bacterial organisms, including viruses, is likely. The antiviral response is triggered by intracellular recognition of viruses via nucleic acid pattern receptors including TLR3 and RIG-I. Activation of these receptors induces an initial type I/III IFN synthesis which subsequently boosts its own production in a positive feedback loop (17). It has been shown that respiratory epithelial cells produce mainly type III IFN and the importance of these proteins in the airways is well-documented (18, 19). Moreover, manipulation of type III IFN has been linked to increased susceptibility of asthmatic patients toward human rhinoviruses (hRV) and a contribution to pulmonary exacerbation has been suggested (20, 21). Since P. aeruginosa and respiratory viruses have been linked to pulmonary exacerbations and in addition, respiratory viruses have been associated with the transition from transient to chronic airway infections with P. aeruginosa (22, 23) a link between both microorganisms is likely. Therefore, we investigated in this study if P. aeruginosa is able to modulate the antiviral response of bronchial epithelial cells and how such interplay might happen at the mechanistical level. In addition we analyzed sputa of CF patients for the presence of respiratory viruses and determined the levels of virus RNA in order to link P. aeruginosa to virus infection thus identifying clinical importance of the experimental findings.