Koike S, Ise I, Sato Y, Yonekawa H, Gotoh O, Nomoto A
Department of Microbiology, Tokyo Metropolitan Institute of Medical Science, Japan.
J Virol. 1992 Dec;66(12):7059-66. doi: 10.1128/JVI.66.12.7059-7066.1992.
Using cDNA of the human poliovirus receptor (PVR) as a probe, two types of cDNA clones of the monkey homologs were isolated from a cDNA library prepared from an African green monkey kidney cell line. Either type of cDNA clone rendered mouse L cells permissive for poliovirus infection. Homologies of the amino acid sequences deduced from these cDNA sequences with that of human PVR were 90.2 and 86.4%, respectively. These two monkey PVRs were found to be encoded in two different loci of the genome. Evolutionary analysis suggested that duplication of the PVR gene in the monkey genome had occurred after the species differentiation between humans and monkeys. The NH2-terminal immunoglobulin-like domain, domain 1, of the second monkey PVR, which lacks a putative N-glycosylation site, mediated poliovirus infection. In addition, a human PVR mutant without N-glycosylation sites in domain 1 also promoted viral infection. These results suggest that domain 1 of the monkey receptor also harbors the binding site for poliovirus and that sugar moieties possibly attached to this domain of human PVR are dispensable for the virus-receptor interaction.
以人脊髓灰质炎病毒受体（PVR）的cDNA为探针，从非洲绿猴肾细胞系构建的cDNA文库中分离出两种猴同源物的cDNA克隆。任一种cDNA克隆都能使小鼠L细胞对脊髓灰质炎病毒感染敏感。从这些cDNA序列推导的氨基酸序列与人PVR的氨基酸序列同源性分别为90.2%和86.4%。发现这两种猴PVR基因定位于基因组的两个不同位点。进化分析表明，猴基因组中PVR基因的复制发生在人与猴物种分化之后。第二种猴PVR的NH2末端免疫球蛋白样结构域（结构域1）缺乏一个假定的N-糖基化位点，但介导脊髓灰质炎病毒感染。此外，在结构域1中没有N-糖基化位点的人PVR突变体也能促进病毒感染。这些结果表明，猴受体的结构域1也含有脊髓灰质炎病毒的结合位点，并且人PVR该结构域上可能连接的糖基部分对于病毒-受体相互作用是可有可无的。
