Search

To gain a better understanding of the genetic changes required for attenuation of duck enteritis virus (DEV), the Chinese standard challenge strain of DEV (DEV CSC) was serially passaged 80 times in chick embryo fibroblasts. We plaque-purified the virus after the 25th passage (DEV p25) and the 80th passage (DEV p80) and investigated its in vitro and in vivo properties. Average plaque sizes for DEV p25 and p80 were significantly smaller than those for their parental DEV CSC. The results from an in vivo experiment revealed that DEV p25 and p80 were avirulent in ducks and protected them from virulent DEV challenge. The complete genome sequence of DEV p80 was determined and compared with that of the parent virus. An 1801-bp deletion was identified in the genome of DEV p80, which affected the genes encoding gI and gE. Moreover, there were 11 base substitutions, which led to seven amino acid changes in open reading frames LORF9, UL51, UL9, UL7, UL4, ICP4 and US3. Further DNA sequence analysis showed that the 1801-bp deletion was also present in DEV p25. Our findings suggest that DEV gE and/or gI are nonessential for virus growth and might, as with other herpesviruses, play an important role in cell-to-cell spread and virulence. Our experiments provide more genetic information about DEV attenuation and further advance our understanding of the molecular basis of DEV pathogenesis. [ABSTRACT FROM AUTHOR]

Here, we present the complete genomic sequence of an attenuated duck enteritis virus (DEV). The Chinese standard challenge strain of DEV (DEV CSC) was serially passaged 20 times in chick embryo fibroblasts and then 85 times in chick embryos. The virus was attenuated and was avirulent to 2-month-old ducks. The attenuated DEV genome is 162,131 base pairs (bp) in length and as long as the parental genomic sequence. There are only 22 nucleotide substitutions, resulting in single amino acid changes in open reading frames LORF5, LORF4, UL41, UL39, UL32, UL13, UL10, UL3, US3, US4 and US7. The genome sequence has been deposited in the GenBank database under accession number KU216226. This study provides genetic information about DEV attenuation and further advances our understanding of the molecular basis of DEV pathogenesis. [ABSTRACT FROM AUTHOR]