During the last decades, it has become evident that viral infections, particularly those caused by human rhinoviruses (RV) are the most frequent triggers of acute exacerbations of asthma; in some cases viral agents have been detected in more than 90% of such events. RVs are also responsible for the majority of mild rhinitis, i.e. common colds, therefore contributing further to symptomatology in respiratory allergic patients. More recently, using prospective study designs, RV infections have also emerged as major determinants for the development of persistent wheeze/asthma.
However, many critical questions remain unanswered in respect to the possibility that one or more infections may drive inflammatory responses towards an unresolved state, including the role of specific microorganisms and/or interactions between such, the role of the immune system in controlling or resolving inflammation and of course the effects of additional, synergistic, possibly subclinical factors. The most significant bottlenecks in the field are:
- Lack of understanding of the relative role of single versus repeated infections in the triggering of chronic inflammation
- Lack of understanding of the role of specific pathogens, pathogen subtypes and interactions between microbial infections
- Inadequate knowledge on the effects of RV infections on the regulatory functions of the immune system
- No knowledge on the mechanisms of resolution of RV-induced inflammation
- Minimal availability of appropriate and predictive pre-clinical models of human disease persistence
- Lack of validated diagnostic or prognostic approaches.
- Nascent translational research in the field of diagnostics and prophylactic interventions
1) to evaluate the hypothesis that repeated infections reprogram the immune system towards a persistent inflammatory pattern leading to respiratory allergies;
2) understand the role of pathogens, altered host-pathogen interactions and mechanisms involved;
3) develop relevant diagnostic and therapeutic strategies.