Agricultural Research Service, U.S. Department of Agriculture, Plum Island Animal Disease Center, Greenport, New York, USA.
Virology. 2010 Sep 15;405(1):149-56. doi: 10.1016/j.virol.2010.05.036. Epub 2010 Jun 30.
Picornavirus RNA replication is initiated by a small viral protein primer, 3B (also known as VPg), that is covalently linked to the 5' terminus of the viral genome. In contrast to other picornaviruses that encode a single copy of 3B, foot-and-mouth disease virus (FMDV) encodes three copies of 3B. Viruses containing disrupted native sequence or deletion of one of their three 3B proteins were derived from a FMDV A24 Cruzeiro full-length cDNA infectious clone. Mutant viruses had growth characteristics similar to the parental virus in cells. RNA synthesis and protein cleavage processes were not significantly affected in these mutant viruses. Cattle infected by aerosol exposure with mutant viruses developed clinical disease similar to that caused by the parental A24 Cruzeiro. Therefore, severe domain disruption or deletion of individual 3B proteins in FMDV do not affect the virus' ability to replicate in vitro and cause clinical disease in cattle.
小核糖核酸病毒的 RNA 复制是由一个小的病毒蛋白引物 3B（也称为 VPg）引发的，该引物与病毒基因组的 5' 末端共价连接。与其他编码单个 3B 拷贝的小核糖核酸病毒不同，口蹄疫病毒（FMDV）编码三个 3B 拷贝。含有破坏的天然序列或缺失其三个 3B 蛋白之一的病毒是从 FMDV A24 Cruzeiro 全长 cDNA 感染性克隆衍生而来的。突变病毒在细胞中的生长特征与亲本病毒相似。这些突变病毒的 RNA 合成和蛋白切割过程没有受到显著影响。用突变病毒通过气溶胶暴露感染的牛会出现类似于由亲本 A24 Cruzeiro 引起的临床疾病。因此，在 FMDV 中严重的结构域破坏或单个 3B 蛋白的缺失不会影响病毒在体外复制和引起牛临床疾病的能力。
