Sivadon V, Lebon P, Rozenberg F
Laboratoire de virologie, Hopital Saint-Vincent de Paul et Université René Descartes, Paris, France.
J Neurovirol. 1998 Feb;4(1):106-14. doi: 10.3109/13550289809113488.
The factors which cause herpes simplex encephalitis (HSE) to occur among herpes simplex virus type 1 (HSV-1) infected humans are not understood. In experimental models, HSV-1 neuroinvasiveness is influenced by amino acid changes in HSV glycoproteins D (gD) or B (gB), which are essential to the virus infectivity and to the induction of host immune responses. To test the possible involvement of these glycoproteins in human HSE, we compared CSF-derived sequences of these genes with those obtained from peripheral HSV-1 isolates. We have previously shown the conservation of gD in 10 HSE samples. Here, we show that the functional domains of gB involved in cell penetration and cell fusion, and the major antigenic domains D2a, D2b and Dd5a were highly conserved. In the gB amino-terminal domain, we distinguished several alleles that were common to HSE and peripheral isolates, and identified in only three out of fifteen HSE cases, a variation that was not encountered in 20 control strains. Overall, there were no striking differences between peripheral and HSE gBs. These results suggest that gB alone may not be responsible for neuroinvasiveness nor human neuropathogenicity.
1型单纯疱疹病毒（HSV - 1）感染人类后导致单纯疱疹性脑炎（HSE）发生的因素尚不清楚。在实验模型中，HSV - 1的神经侵袭性受HSV糖蛋白D（gD）或B（gB）中氨基酸变化的影响，这些糖蛋白对病毒感染性及宿主免疫反应的诱导至关重要。为了测试这些糖蛋白是否可能参与人类HSE的发生，我们将这些基因在脑脊液中获得的序列与从外周HSV - 1分离株中获得的序列进行了比较。我们之前已证明10份HSE样本中gD的保守性。在此，我们表明，gB中参与细胞穿透和细胞融合的功能结构域以及主要抗原结构域D2a、D2b和Dd5a高度保守。在gB氨基末端结构域，我们区分出几种HSE和外周分离株共有的等位基因，并且在15例HSE病例中仅3例发现了一种在20株对照菌株中未出现的变异。总体而言，外周和HSE的gB之间没有显著差异。这些结果表明，单独的gB可能不是神经侵袭性和人类神经致病性的原因。
