Duan Zhiqiang, Hu Zenglei, Zhu Jie, Xu Haixu, Chen Jian, Liu Huimou, Hu Shunlin, Liu Xiufan
Animal Infectious Disease Laboratory, College of Veterinary Medicine, Yangzhou University, 12 East Wenhui Road, Yangzhou, 225009, Jiangsu, China.
Arch Virol. 2014 Jul;159(7):1813-9. doi: 10.1007/s00705-014-1998-2. Epub 2014 Jan 30.
The FPIV-like late domains identified in the matrix (M) proteins of parainfluenza virus 5 and mumps virus have been demonstrated to be critical for virus budding. In this study, we found that the same FPIV sequence motif is present in the N-terminus of the Newcastle disease virus (NDV) M protein. Mutagenesis experiments demonstrated that mutation of either phenylalanine (F) or proline (P) to alanine led to a more obvious decrease in viral virulence and replication and resulted in poor budding of the mutant viruses. Additionally, evidence for the involvement of cellular multivesicular body (MVB) proteins was obtained, since NDV production was inhibited upon expression of dominant-negative versions of the VPS4A-E228Q protein. Together, these results demonstrate that the FPIV motif, especially the residues F and P, within the NDV M protein, plays a critical role in NDV replication and budding, and this budding process likely involves the cellular MVB pathway.
在副流感病毒5和腮腺炎病毒的基质（M）蛋白中鉴定出的类FPIV晚期结构域已被证明对病毒出芽至关重要。在本研究中，我们发现新城疫病毒（NDV）M蛋白的N端存在相同的FPIV序列基序。诱变实验表明，将苯丙氨酸（F）或脯氨酸（P）突变为丙氨酸会导致病毒毒力和复制更明显下降，并导致突变病毒出芽不良。此外，由于表达VPS4A - E228Q蛋白的显性负性形式会抑制NDV产生，因此获得了细胞多囊泡体（MVB）蛋白参与的证据。总之，这些结果表明，NDV M蛋白中的FPIV基序，尤其是F和P残基，在NDV复制和出芽中起关键作用，并且这种出芽过程可能涉及细胞MVB途径。
