Protection of guinea pigs from primary and recurrent herpes simplex virus (HSV) type 2 cutaneous disease with vaccinia virus recombinants expressing HSV glycoprotein D.

Protection of guinea pigs from primary and recurrent herpes simplex virus (HSV) type 2 cutaneous disease with vaccinia virus recombinants expressing HSV glycoprotein D.
复制标题

使用表达 HSV 糖蛋白 D 的痘苗病毒重组体保护豚鼠免受原发性和复发性单纯疱疹病毒 (HSV) 2 型皮肤病的影响。

DOI:
10.1093/infdis/155.6.1188
复制
发表时间:
1987
期刊:
The Journal of infectious diseases
影响因子:
--
通讯作者:
Paoletti,E
Paoletti,E
中科院分区:
--
文献类型:
--
作者:
Wachsman,M;Aurelian,L;Smith,CC;Lipinskas,BR;Perkus,ME;Paoletti,E

文献摘要

被引文献

相似文献

研究了含有单纯疱疹病毒(HSV)1型(VP 176)或2型(VP 221)糖蛋白D(gD)基因的重组痘苗病毒在复发性HSV 2型疾病豚鼠模型中的保护潜力。用这些重组体感染的细胞合成至少一种蛋白质(前体、成熟形式或两者),该蛋白质用单克隆抗体沉淀到gD上的HSV型共同决定簇。在感染后2小时,在用重组体感染的细胞表面上检测到这些决定簇。VP 176免疫保护免受原发性(P <0.001)和复发性(P <0.001)HSV 2型皮肤损害和神经节潜伏期(62%保护)。VP 221免疫对复发性疾病有保护作用(P<0.05),尽管HSV 2型神经节细胞感染已建立。在免疫后两周首次观察到的保护显然不涉及HSV特异性中和抗体,因为在免疫后35-45天检测到血清转化。保护作用与HSV特异性淋巴细胞增殖和增强自然杀伤细胞溶解的淋巴因子的产生有关。
Vaccinia virus recombinants containing herpes simplex virus (HSV) type 1 (VP176) or type 2 (VP221) glycoprotein D (gD) genes were studied for their protective potential in the guinea pig model of recurrent HSV type 2 disease. Cells infected with these recombinants synthesized at least one protein (precursor, mature form, or both) that was precipitated with monoclonal antibody to HSV type-common determinants on gD. These determinants were detected on the surface of cells infected with the recombinants at 2 hr after infection. VP176 immunization protected against primary (P⪡ .001) and recurrent (P⪡ .001) cutaneous HSV type 2 lesions and ganglionic latency (62% protection). VP221 immunization protected against recurrent disease (P< .05), although HSV type 2 gan-glionic infection was established. Protection, first observed at two weeks after immunization, apparently did not involve HSV-specific neutralizing antibody because seroconversion was detected at 35–45 days after immunization. Protection was correlated with HSV-specific lymphoproliferation and the elaboration of lymphokines that enhance natural killer cell cytolysis.