It has been shown that HBoV1 remains detectable in the upper airways of patients for weeks and months, even up to half a year [68] [69] [70] [71] . However, the mechanism behind this persistence, i.e. whether it is due to persistent replication and shedding, passive persistence after primary infection, or recurrent mucosal surface contamination, has remained unknown. Our results in in vitro HAE cultures showed that HBoV1 is able to replicate and shed from both the apical and basolateral surfaces at least for three weeks, supporting the notion that shedding of the virus from the airways is a long-lasting process. This may further explain why a high rate of co-infection, or co-detection, between HBoV1 and other respiratory viruses has been reported [5] . Since recombinant AAV persists as an episome in transduced tissues, which prolongs gene expression [72, 73] , it is possible that also the HBoV1 genome can be presented as an episome [29, 30] for long term expression and replication. Apparently, the mechanism underlying this feature of HBoV1 infection warrants further investigation. However, in contrast to the other human-pathogenic B19V, HBoV1 does not seem to persist in human tissues for many years [74] .