Of the 324 HBoV positive samples, 106 (32.7%) were genotyped in the type-specific assays. HBoV-1 was found predominantly in controls (p,0.001) and the prevalence of HBoV-3 was similar in cases and controls. Both HBoV-1 and -3 were predominantly found in children. HBoV-2 was predominantly associated with gastroenteritis cases (p,0.01). The overall prevalence in cases was 1.4% and 0.8% in controls, however, in children ,5 year of age, the prevalence in cases and controls was similar, 2.8% and 2.6%, respectively. The prevalence of HBoV-2 in children in the UK was significantly lower than that reported in a study in Australia, in which HBoV-2 was detected in 17.2% and 8.1% of the cases and controls, respectively [22] . The findings of the study in Australia lead to the proposal of HBoV-2 as an important aetiological agent of infantile gastroenteritis. It is noteworthy however, that in the Australian study, the association of HBoV-2 with gastroenteritis was only significant when cases with a bacterial co-pathogen were included in the analysis. Although in the present study HBoV-2 in the absence of other enteric pathogens was found more frequently in cases than in controls, the small numbers found in such large study suggest that the role of these viruses in IID, if any, is likely to be small. A lack of correlation between HBoVs or HBoV-2 and paediatric gastroenteritis was also reported in several smaller studies published elsewhere [30, 31, 32] . A total of 67% of the HBoV-positive samples could not be genotyped using the genotype-specific PCR assays. The majority of these untyped samples (70%) had CT values .37. This suggests that failure to type may be associated with low viral loads and differences in the relative sensitivities of the genotyping assays compared to the detection assay. Although under experimental conditions and using plasmid controls the sensitivities of all assays were comparable, it is likely that when applied to true clinical samples the sensitivity of the type-specific assays was inferior, possibly due to as yet not identified strain variability within genotypes. Also, a HBoV type 4-specific assay was not included in this study, therefore, any possible HBoV4 infections would not have been typed. Of the panel of samples that were tested in an alternative pan-HBoV PCR, the strains typed through sequencing were HBoV-1 (2 samples), HBoV-2 (1 sample) and HBoV-3 (3 samples). Furthermore, the distribution of untyped HBoVs was not significantly different in cases and controls.