Wachsman M, Aurelian L, Hunter J C, Perkus M E, Paoletti E
Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore 21201.
Biosci Rep. 1988 Aug;8(4):323-34. doi: 10.1007/BF01115223.
We studied the effect of the temporal regulation of herpes simplex virus (HSV) type 1 glycoprotein D (gD-1) expression in Ia+ epidermal cells (EC) and macrophages on virus specific immunity and protection from HSV-2 challenge. gD-1 was expressed on the surface of cells infected with a vaccinia recombinant containing gD-1 under the control of an early vaccinia virus promoter (VP176). It was not expressed in cells infected with a recombinant (VP254) in which gD-1 is controlled by a late vaccinia virus promoter. BALB/c mice immunized with both recombinants seroconverted to HSV-2 as determined by neutralization. However, HSV specific delayed type hypersensitivity (DTH) responses were significantly (p less than 0.025) higher in VP176 than VP254 immunized animals. Both VP176 and VP254 immunized mice were protected from severe neurological disease due to HSV-2 challenge at 14 days post immunization, but long term protection was observed only in VP176 immunized mice.
我们研究了单纯疱疹病毒1型糖蛋白D（gD-1）在Ia⁺表皮细胞（EC）和巨噬细胞中的表达时间调控对病毒特异性免疫以及抵御HSV-2攻击的保护作用。gD-1在感染了痘苗重组病毒的细胞表面表达，该重组病毒含有在早期痘苗病毒启动子（VP176）控制下的gD-1。在感染了重组病毒（VP254）的细胞中gD-1不表达，在VP254中gD-1由晚期痘苗病毒启动子控制。用两种重组病毒免疫的BALB/c小鼠通过中和试验检测显示血清转化为HSV-2阳性。然而，VP176免疫的动物中HSV特异性迟发型超敏反应（DTH）显著（p小于0.025）高于VP254免疫的动物。在免疫后14天，VP176和VP254免疫的小鼠均受到保护，免受HSV-2攻击导致的严重神经疾病，但仅在VP176免疫的小鼠中观察到长期保护作用。
