Identification of sequence changes in live attenuated goose parvovirus vaccine strains developed in Asia and Europe

• Published in: Avian pathology 2008-10, Vol.37 (5), p.499-505
• Main Authors: Shien, J.-H., Wang, Y.-S., Chen, C.-H., Shieh, H.K., Hu, C.-C., Chang, P.-C.
• Format: Article
• Language: English
• Subjects: Amino Acid Sequence; Amino acids; Animal vaccines; Animals; Asia; Base Sequence; Capsid Proteins - chemistry; Capsid Proteins - genetics; Comparative analysis; Europe; Geese - virology; Genome, Viral; Mutation; Parvovirus - genetics; Viral Nonstructural Proteins - chemistry; Viral Nonstructural Proteins - genetics; Viral Vaccines - immunology; Viruses; Wildfowl
• ISSN: 0307-9457; 1465-3338
• DOI: 10.1080/03079450802356979

Live attenuated vaccines have been used for control of the disease caused by goose parvovirus (GPV), but the mechanism involved in attenuation of GPV remains elusive. This report presents the complete nucleotide sequences of two live attenuated strains of GPV (82-0321V and VG32/1) that were independently developed in Taiwan and Europe, together with the parental strain of 82-0321V and a field strain isolated in Taiwan in 2006. Sequence comparisons showed that 82-0321V and VG32/1 had multiple deletions and substitutions in the inverted terminal repeats region when compared with their parental strain or the field virus, but these changes did not affect the formation of the hairpin structure essential for viral replication. Moreover, 82-0321V and VG32/1 had five amino acid changes in the non-structural protein, but these changes were located at positions distant from known functional motifs in the non-structural protein. In contrast, 82-0321V had nine changes and VG32/1 had 11 changes in their capsid proteins (VP1), and the majority of these changes occurred at positions close to the putative receptor binding sites of VP1, as predicted using the structure of adeno-associated virus 2 as the model system. Taken together, the results suggest that changes in sequence near the receptor binding sites of VP1 might be responsible for attenuation of GPV. This is the first report of complete nucleotide sequences of GPV other than the virulent B strain, and suggests a possible mechanism for attenuation of GPV.