Recurrent rhinovirus infections in a child with inherited MDA5 deficiency

Lamborn, Ian T.; Jing, Huie; Zhang, Yu; Drutman, Scott B.; Abbott, Jordan K.; Munir, Shirin; Bade, Sangeeta; Murdock, Heardley M.; Santos, Celia P.; Brock, Linda G.; Masutani, Evan; Fordjour, Emmanuel Y.; McElwee, Joshua J.; Hughes, Jason D.; Nichols, Dave P.; Belkadi, Aziz; Oler, Andrew J.; Happel, Corinne S.; Matthews, Helen F.; Abel, Laurent; Collins, Peter L.; Subbarao, Kanta; Gelfand, Erwin W.; Ciancanelli, Michael J.; Casanova, Jean-Laurent; Su, Helen C.

Because HRV/enterovirus infection preceded the onset of chronic lung disease and HRV/enterovirus infections frequently precipitated hospitalization, we molecularly typed positive samples from the proband. RT-PCR and sequencing of the conserved 5′ UTR used primers that preferentially amplify HRV species A, B, and C and distinguish between HRV and enterovirus (Bochkov et al., 2014) . Analysis of PCR-amplified products from seven nasopharyngeal samples collected sequentially from the patient over a 2-yr window demonstrated shedding of HRV-A, but not -B or -C (Fig. 1 , B and C). Each sample contained only one HRV-A serotype from 96 clones sequenced, and no two samples (excepting "b" and "c" which were collected within five d of each other) contained the same serotype. Phylogenetic analysis did not reveal any clustering of the identified serotypes ( Fig. 1 C) . Thus, the frequent detection of HRV/enterovirus was not caused by defective clearance of individual serotypes, but rather resulted from frequent infection with unrelated HRV serotypes.