The high frequency of HBoV detection (43%) in our asymptomatic children contrasts with the results of the few other studies that included a control group of asymptomatic children. Fry et al. (10) detected HBoV DNA in only 1% of nasal swabs from asymptomatic patients. Maggi et al. (16) did not detect HBoV DNA in nasal swabs from 51 asymptomatic children (including 30 healthy infants with a mean age of 6 months and 21 preadolescent healthy children with a mean age of 12.8 years). However, these studies analyzed nasal swabs instead of NPA or BAL samples for HBoV detection, which may result in lower rates of viral detection, as shown in symptomatic persons. Allander et al. (2) did not detect HBoV in any of 64 asymptomatic children (median age 4.1 years, range 5 months to 14 years) but used nasal swabs in asymptomatic patients and NPA samples in symptomatic patients. Furthermore, their control group was also older than our population (mean 18.6 months, median 18 months). Kesebir DNA in nasal washes from 96 asymptomatic children <2 years of age seen at a clinic compared with 22 (5.2%) of 425 various samples from symptomatic children sent to a hospital clinical laboratory. None of the previous studies used a control group consisting of children matched for age and week of admission and analyzed the same type of respiratory samples for cases and controls. Our positive results for HBoV were confi rmed by using 2 sets of PCR primers targeting different genes (NP1 and NS1) in a duplex PCR assay and by subsequent testing with a third set of primers (VP1/VP2) for sequencing. Also, sample preparation and PCR amplifi cation were performed in separate laboratory areas following the stringent quality control program of our institution. Thus, it is unlikely that our positive results were due to PCR cross-contamination. Our method was also very sensitive (detection limit = 10 genome copies), which probably enabled an increased in-fection rate compared with previous reports. We cannot exclude the possibility that prior RTIs (in the few weeks preceding sampling) occurred in our asymptomatic children hospitalized for an elective surgery or that HBoV could establish a prolonged infection in children compared with other respiratory viruses. However, the 3× higher detection rate in controls than in symptomatic children make these explanations unlikely. We did not quantify HBoV DNA load in samples from our study, which could have been different between asymptomatic and symptomatic children. Nevertheless, we detected hRSV, hMPV, and infl uenza virus RNA in <1% of the same NPA samples from those asymptomatic children compared with a rate of 43% for HBoV DNA (25) . At the very least, our results should raise concerns about the pathogenic role of HBoV in children.