Complete genome sequence of canine astrovirus with molecular and epidemiological characterisation of UK strains.
Bottom Line: These viruses can also cause infection in a range of domestic and wild animal species.Sequencing of the capsid sequences from the four CaAstV strains found significant genetic heterogeneity, with only 80% amino acid identity between strains.The full genome sequence of two UK CaAstV strains was then determined, confirming that CaAstV conforms to the classic genome organisation of other astroviruses with ORF1a and ORF1b separated by a frameshift and ORF2 encoding the capsid protein.
Affiliation: Division of Virology, Department of Pathology, University of Cambridge, Addenbrookes Hospital, Cambridge CB2 2QQ, UK; Section of Virology, Faculty of Medicine, Imperial College London, St. Mary's Campus, London W2 1PG, UK. Electronic address: firstname.lastname@example.org.Show MeSH
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Mentions: A number of studies have reported the N-terminal and C-terminal regions of astrovirus capsids to be relatively conserved, whereas the central region is hypervariable. The human astrovirus capsid protein has previously been divided into three regions; the N terminus (amino acids 1–415), a variable central region (416–707), which includes a hypervariable section from 649 to 707, and a conserved C terminus (708–786) (Willcocks et al., 1995). An analogous approach for the CaAstV capsid was taken by Zhu et al. (2011), who divided the capsid into three regions for analysis: amino acids 1–446, 447–730, and 731–end. The four capsid sequences derived from this study have been analysed according to the latter scheme, and sequence identity compared (Fig. 1). Sequence analysis of the three regions clearly shows that the majority of sequence variation is concentrated in region II. A 24 nt deletion was identified in samples 2–4 in the 5′ end region II, which has previously been reported in Chinese CaAstV strains (Zhu et al., 2011). It is not possible to predict the location of this deletion on the capsid structure as it is beyond the region of the astrovirus capsid spike for which the crystal structure has been solved (Dong et al., 2011). However, sequence alignment with the human astrovirus type 8 capsid (GenBank AAF85964.1) shows this deletion to be located downstream of the caspase cleavage site required for virion maturation, which truncates the full length capsid protein (VP90) into the mature VP70 form (Banos-Lara and Méndez, 2010). Therefore it is predicted that the 24 nt deletion will not alter the mature virion.
Affiliation: Division of Virology, Department of Pathology, University of Cambridge, Addenbrookes Hospital, Cambridge CB2 2QQ, UK; Section of Virology, Faculty of Medicine, Imperial College London, St. Mary's Campus, London W2 1PG, UK. Electronic address: email@example.com.