For most viral infections, disease severity is the result of a close interplay between viral and host factors. The host immune status is known to play a critical role for viral clearance and resolution of infection. Abnormal innate immune responses to HRV have been observed in individuals presenting HRV-induced COPD or asthma exacerbation [11, 12] . By contrast, reports are rare on the implication of viral determinants in HRV disease severity. Palmemberg et al proposed that the rhinovirus 59UTR polypyrimidine tract may affect virulence [13] . At the serotype or species level, a clear association between the genotype and induced pathology remains to be demonstrated. HRVs were previously classified into two species, HRV-A and HRV-B. In 2006, a third species, HRV-C, was identified [14, 15, 16, 17, 18, 19] and appears to be highly prevalent and circulating worldwide [20, 21, 22] . Several studies have suggested that HRV-C types are prone to induce more severe illness in children [17, 21, 23, 24, 25] .