Fleming J O, Trousdale M D, el-Zaatari F A, Stohlman S A, Weiner L P
J Virol. 1986 Jun;58(3):869-75. doi: 10.1128/JVI.58.3.869-875.1986.
To analyze the pathogenesis of the neurotropic murine coronavirus JHMV, we used monoclonal antibodies to the E2 viral glycoprotein to select antigenic variant viruses. Monoclonal antibodies J.7.2 and J.2.2 were shown to bind to topographically distinct regions of the E2 molecule, and the variants selected with the two antibodies demonstrated very different disease pictures in mice. Variants selected with J.7.2 were, like the parental virus, highly virulent and caused an acute encephalitic illness. By contrast, J.2.2-selected variants predominantly caused a subacute paralytic disease clinically and extensive demyelination histologically. Antigenic differences among the variants and parental virus were readily demonstrable with anti-E2 monoclonal antibodies. However, no differences between the viruses could be shown in binding studies with monoclonal antibodies directed against either E1 or N, the other two JHMV structural proteins. Since only J.2.2 selected demyelinating variants with reduced neurovirulence, it is likely that this monoclonal antibody recognizes a subregion of the E2 molecule that is particularly important in JHMV pathogenesis.
为分析嗜神经性鼠冠状病毒JHMV的发病机制，我们使用针对E2病毒糖蛋白的单克隆抗体来筛选抗原变异病毒。单克隆抗体J.7.2和J.2.2被证明可结合到E2分子的不同拓扑区域，用这两种抗体筛选出的变异病毒在小鼠中表现出非常不同的疾病情况。用J.7.2筛选出的变异病毒与亲代病毒一样，具有高致病性，可引发急性脑炎性疾病。相比之下，用J.2.2筛选出的变异病毒在临床上主要引发亚急性麻痹性疾病，在组织学上表现为广泛的脱髓鞘。抗E2单克隆抗体很容易证明变异病毒和亲代病毒之间的抗原差异。然而，用针对另外两种JHMV结构蛋白E1或N的单克隆抗体进行的结合研究中，未显示出病毒之间的差异。由于只有J.2.2筛选出了神经毒力降低的脱髓鞘变异病毒，因此这种单克隆抗体可能识别出E2分子中在JHMV发病机制中特别重要的一个亚区域。
