Beard Philippa M, Froggatt Graham C, Smith Geoffrey L
Department of Virology, Faculty of Medicine, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK.
J Gen Virol. 2006 Jun;87(Pt 6):1521-1529. doi: 10.1099/vir.0.81854-0.
The vaccinia virus (VACV) protein A55 is a BTB/kelch protein with a broad-complex, tramtrack and bric-a-brac (BTB) domain in the N-terminal region and five kelch repeats in the C-terminal half. The BTB/kelch subgroup of the kelch superfamily of proteins has been associated with a wide variety of functions including regulation of the cytoskeleton. VACV contains three genes predicted to encode BTB/kelch proteins: A55R, F3L and C2L. The A55R gene product has been identified as an intracellular protein of 64 kDa that is expressed late in infection. A VACV strain lacking 93.6% of the A55R open reading frame (vdeltaA55) was constructed and found to have an unaltered growth rate in vivo but a different plaque morphology and cytopathic effect, as well as reduced development of VACV-induced Ca2+-independent cell/extracellular matrix adhesion. In a murine intradermal model of VACV infection, a virus lacking the A55R gene induced larger lesions than wild-type and revertant control viruses.
痘苗病毒（VACV）蛋白A55是一种BTB/kelch蛋白，其N端区域有一个广泛复合体、轨道和杂乱（BTB）结构域，C端有五个kelch重复序列。kelch蛋白超家族的BTB/kelch亚组与多种功能相关，包括细胞骨架的调节。VACV包含三个预测编码BTB/kelch蛋白的基因：A55R、F3L和C2L。A55R基因产物已被鉴定为一种64 kDa的细胞内蛋白，在感染后期表达。构建了一个缺失93.6% A55R开放阅读框的VACV毒株（vdeltaA55），发现其在体内生长速率未改变，但噬斑形态和细胞病变效应不同，以及VACV诱导的不依赖Ca2+的细胞/细胞外基质黏附的发展减少。在VACV感染的小鼠皮内模型中，缺失A55R基因的病毒比野生型和回复对照病毒诱导的损伤更大。
