A single amino acid V4I substitution in VP1 attenuates virulence of very virulent infectious bursal disease virus (vvIBDV) in SPF chickens and increases replication in CEF cells

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• 作者：Fei Yu ; Xiangang Ren ; Yongqiang Wang ; Xiaole Qi ; Jiasheng Song ; Yulong Gao ; Liting Qin ; Honglei Gao ; Xiaomei Wang ; ^{xmw@hvri.ac.cn}
• 关键词：VvIBDV ; VP1 ; Replication ; Pathogenicity
• 刊名：Virology
• 出版年：2013
• 出版时间：5 June, 2013
• 年：2013
• 卷：440
• 期：2
• 页码：204-209
• 全文大小：363 K

文摘

Infectious bursal disease virus (IBDV) is a birnavirus that causes immunosuppressive disease in chickens. The emergence of very virulent IBDV (vvIBDV) has brought new challenges for this disease. The molecular determinants for the high pathogenicity of vvIBDV are not fully understood. Previous studies focused mostly on the VP2 protein on segment A, but recent evidence suggests that segment B also plays an important role. Previously we identified eight amino acid changes in the VP1 protein of vvIBDV. In this study, we investigated effect of amino acids substitutions in VP1 on viral replication and pathogenicity. We identified a Valine to Isoleucine substitution at amino acid position 4 (V4I) of VP1 that attenuates viral pathogenicity and reduces viral replication in SPF chickens but increases viral replication in CEF cells. This study confirms that VP1 of segment B play an important role in viral replication and pathogenicity of vvIBDV.