Taken together, our data suggest that immunocompromised patients cannot clear viral infections as immunocompetent individuals, and represent a potential reservoir for the emergence of new variants and inter-host transmission due to longer chronic viral infection. In addition, these patients may be co-infected by two viruses, thus opening the door to recombination, another putative driving force of rhinovirus evolution [30] . With the emergence of new therapies and progress in transplantation, the population of immunocompromised patients is constantly increasing. Our results suggest that this could accelerate the ability of viruses to adapt to the host, evolve, and propagate and may favor a more rapid emergence of new viral variants. Figure S1 Repartition of protracted and lower respiratory tract infections among the HRV-A (panel A), HRV-B (panel B), and HRV-C (panel C) reference serotypes. VP4-VP2 cladograms of rhinoviruses isolated from lung transplant recipients (blue) and routinely screened hospital patients (red) (Table S1), as well as the 74 HRV-A (panel A), 25 HRV-B (panel B), and 61 proposed HRV-C reference types (black) (panel C). SV1 (GenBank accession number AY064708) was used as an outgroup. LRT and PI are highlighted by arrows and black lines respectively. (PDF)