Reproduction and pathogenesis of short beak and dwarfish syndrome in Cherry Valley Pekin ducks infected with the rescued novel goose parvovirus

文献类型： 外文期刊

第一作者： Wang, Jianye

作者： Wang, Jianye;Wang, Yu;Li, Yonglin;Jiang, Zhiwei;Zhu, Guoqiang;Wang, Xiaobo;Wang, Jianye;Wang, Yu;Li, Yonglin;Jiang, Zhiwei;Zhu, Guoqiang;Wang, Xiaobo;Gao, Yuehua;Li, Yufeng

作者机构：

关键词： Goose parvovirus; short beak and dwarfish syndrome; reproduction; pathogenesis; rescue

期刊名称：VIRULENCE （ 影响因子：5.428； 五年影响因子：6.735 ）

ISSN： 2150-5594

年卷期： 2022 年 13 卷 1 期

页码：

收录情况： SCI

摘要： Since the outbreak of short beak and dwarfish syndrome (SBDS) in Cherry Valley Pekin ducks in China, novel goose parvovirus (NGPV) has been isolated. Till now, little is known about the NGPV pathogenesis toward Cherry Valley Pekin ducks. Besides, due to detection of duck circovirus co-infection in SBDS clinical cases, whether sole NGPV infection can reproduce all the typical symptoms of SBDS remains unclear. In this study, based on the NGPV isolate SDJN19, an infectious plasmid clone pJNm containing the entire SDJN19 genome was constructed. Transfection of pJNm in embryonated duck eggs resulted in generation of the infectious virus carrying the genetic marker, named rJNm. rJNm infection of 2-day-old Cherry Valley Pekin ducks reproduced all the typical signs of SBDS, including beak atrophy, tongue protrusion, and growth retardation. rJNm can infect Cherry Valley Pekin ducks through the horizontal transmission route, and the infected ducks exhibited the characteristic SBDS symptoms. A high level of serum precipitation antibodies (above 5log(2)) were induced in the surviving ducks, however, high viral loads were still detected in the duck organs, suggesting persistent NGPV infection in ducks. By incorporating the homologous Rep1 and VP1 gene from classical GPV, two chimeric viruses rJN-cVP1 and rJN-cRep1 were generated. Duck infection tests revealed that the non-structural protein Rep1 played a crucial role in the NGPV pathogenicity. The present result lays a solid foundation for further exploring how the Rep protein contributes to the NGPV pathogenesis.

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