1c). The nucleotide sequence of the amplicon was identical to that obtained earlier, suggesting that the bird had been persistently infected with ABV5 for at least eight months without developing clinical signs of PDD. Although we tried to isolate ABV5 from the fecal sample with QT6 cells (Japanese quail fibroblast), we did not detect ABV RNA and protein after one month’s passage. Because only partial sequences of the N and M genes of ABV5 have been GS-1101 chemical structure established so far, we tried to determine the nucleotide sequence from the N to M gene (Fig. 2). We carried out PCR with MH192 and 193 primers and amplified the target region

successfully. Sequence analysis showed that the genomic structure of ABV5 (Acc. No. AB519144) is almost identical to that of other bornaviruses. Interestingly, however, the upstream sequence of the X of ABV5 appears to differ from those of other bornaviruses (Fig ALK inhibitor 2). The bornavirus X

and P genes are transcribed as a bicistronic X/P mRNA (11). In BDV, a mammalian bornavirus, the 5′ UTR of the X/P mRNA contains a short uORF, which plays a critical role in translational regulation of the X and P (12–16). On the other hand, 22 nucleotides in this region are absent from ABV2 and 4, resulting in a lack of the uORF (17). Interestingly, although the 5′ UTR sequence of ABV5 X/P mRNA is almost the same length as that of BDV, only the shorter uORF is found in ABV5 (Fig. 2). These observations suggest that, in ABV5, the strategy for regulation of expression of X and P proteins differs from those of other bornaviruses. Of note: during the preparation of this manuscript, a novel genotype of ABV was detected in Canada geese (Branta canadensis) (18). Intriguingly, the 5′ UTR sequence of the X/P mRNA of the Canada geese ABV was shown to encode an uORF three amino acids longer than ABV5. It would be of interest to determine the nucleotide sequences of other genotypes of ABV and to compare the mechanisms of regulation of X and P gene expression among bornaviruses.

In this study, although we detected ABV5 RNA in an Eclectus Amobarbital roratus with FPD, it remains unclear whether ABV5 infection was the cause of the disease. Thus far, several possible causes of FPD have been proposed: infection with microorganisms and parasites, organopathy and psychogenic factors (19). Intriguingly, one of three birds reportedly developed FPD after injection of a brain homogenate containing ABV (7). In the case of BDV infection, two types of clinical course have been identified in a rat model (20). Adult rats inoculated with BDV develop immune cell mediated fatal non-suppurative encephalitis, which is histopathologically similar to PDD. On the other hand, in neonatal rats BDV causes chronic infections, which lead to a milder behavioral syndrome without overt encephalitis. Therefore, it is plausible that ABV infection can cause milder diseases such as FPD.