A PICORNAVIRAL PROTEIN SYNTHESIZED OUT OF FRAME WITH THE POLYPROTEIN PLAYS A KEY ROLE IN A VIRUS-INDUCED IMMUNE-MEDIATED DEMYELINATING DISEASE
A PICORNAVIRAL PROTEIN SYNTHESIZED OUT OF FRAME WITH THE POLYPROTEIN PLAYS A KEY ROLE IN A VIRUS-INDUCED IMMUNE-MEDIATED DEMYELINATING DISEASE
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DOI：
10.1038/nm0995-927
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发表时间：
1995-09-01
期刊：
影响因子：
82.9
通讯作者：
ROOS, RP
中科院分区：
文献类型：
--
作者：
CHEN, HH;KONG, WP;ROOS, RP
泰勒氏鼠脑脊髓炎病毒 (TMEV) 的 DA 株和 TO 亚组的其他成员可诱导一种病毒表达受限的慢性脱髓鞘疾病。这种疾病是多发性硬化症的实验模型；在这两种疾病中，免疫系统都会导致类似的脱髓鞘病理。与所有小核糖核酸病毒一样，TMEV 编码一种从长开放阅读框翻译而来的多蛋白。然后多蛋白被加工成结构和非结构病毒蛋白。在这里，我们证明 TMEV 的 DA 菌株有一个额外的替代开放阅读框，它编码存在于感染细胞中的一种名为 L* 的蛋白质。具有L*突变的病毒的脱髓鞘活性显着降低，表明L*在TO亚群诱导的脱髓鞘疾病中发挥着关键作用。 L* 与膜相关，表明 L* 可能与免疫系统相互作用，从而介导病毒诱导的脱髓鞘疾病。
The DA strain and other members of the TO subgroup of Theiler's murine encephalomyelitis virus (TMEV) induce a chronic demyelinating disease with a restricted virus expression. This disease serves as an experimental model of multiple sclerosis; in both diseases the immune system contributes to a similar demyelinating pathology. Like all picornaviruses, TMEV encodes a polyprotein translated from one long open reading frame. The polyprotein is then processed into structural and non-structural viral proteins. Here, we demonstrate that the DA strain of TMEV has an additional alternative open reading frame that encodes a protein called L* that is present in infected cells. Virus with a mutation of L* has a dramatically decreased demyelinating activity, indicating that L* plays a critical role in TO subgroup-induced demyelinating disease. L* is associated with membranes, suggesting that L* may interact with the immune system and thereby mediate the viral-induced demyelinating disease.