Todd Daniel, Scott Alistair N J, Ball Neris W, Borghmans Borghert J, Adair Brian M
Department of Agriculture and Rural Development for Northern Ireland, Veterinary Sciences Division, the Queen's University of Belfast, Stormont, United Kingdom.
J Virol. 2002 Aug;76(16):8472-4. doi: 10.1128/jvi.76.16.8472-8474.2002.
Chimeric virus experiments indicated that the pathogenicity and monoclonal antibody reactivity differences between two molecularly cloned, highly passaged chicken anemia virus isolates could be attributed to the VP1 amino acid change at residue 89. The introduction of this change into a pathogenic cloned low-passage isolate was not sufficient to cause attenuation.
嵌合病毒实验表明,两种分子克隆的、经过高度传代的鸡贫血病毒分离株之间的致病性和单克隆抗体反应性差异可归因于第89位氨基酸处的VP1氨基酸变化。将此变化引入致病的克隆低传代分离株中不足以导致病毒减毒。