Atwood W J, Norkin L C
Graduate Program in Neuroscience and Behavior, University of Massachusetts, Amhers 01003.
J Virol. 1989 Oct;63(10):4474-7. doi: 10.1128/JVI.63.10.4474-4477.1989.
Class I major histocompatibility complex proteins appear to be the major cell surface receptors for simian virus 40 (SV40), as implied by the following observations. Adsorption of SV40 to LLC-MK2 rhesus monkey kidney cells specifically inhibited binding of a monoclonal antibody (MAb) against class I human lymphocyte antigen (HLA) proteins. Conversely, pretreatment of LLC-MK2 cells with anti-HLA MAbs inhibited infection by SV40. The ability of anti-HLA to inhibit infection was greatly reduced when the order of addition of the anti-HLA and the virus was reversed. Infection was also inhibited by preincubating SV40 with purified soluble class I protein. Finally, human lymphoblastoid cells of the Daudi line, which do not express class I major histocompatibility complex proteins, were infected at relatively low levels with SV40 virions. In a control experiment, we found that pretreatment of cells with a MAb specific for the leukocytic-function-associated antigen LFA-3 actually enhanced infection. This finding may also support the premise that class I major histocompatibility complex proteins are receptors for SV40.
I类主要组织相容性复合体蛋白似乎是猴病毒40（SV40）的主要细胞表面受体，以下观察结果表明了这一点。SV40吸附到LLC-MK2恒河猴肾细胞上会特异性抑制抗I类人类淋巴细胞抗原（HLA）蛋白的单克隆抗体（MAb）的结合。相反，用抗HLA单克隆抗体预处理LLC-MK2细胞可抑制SV40感染。当抗HLA和病毒的添加顺序颠倒时，抗HLA抑制感染的能力会大大降低。用纯化的可溶性I类蛋白预孵育SV40也可抑制感染。最后，不表达I类主要组织相容性复合体蛋白的Daudi系人淋巴母细胞被SV40病毒粒子以相对较低的水平感染。在一项对照实验中，我们发现用针对白细胞功能相关抗原LFA-3的单克隆抗体预处理细胞实际上增强了感染。这一发现也可能支持I类主要组织相容性复合体蛋白是SV40受体的前提。
