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首页> 外文期刊>Japanese journal of infectious diseases >Theiler's murine encephalomyelitis virus (TMEV): the role of a small out-of-frame protein in viral persistence and demyelination.
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Theiler's murine encephalomyelitis virus (TMEV): the role of a small out-of-frame protein in viral persistence and demyelination.

机译:泰勒氏鼠脑脊髓炎病毒(TMEV):一种小框外蛋白在病毒持续性和脱髓鞘中的作用。

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摘要

Theiler's murine encephalomyelitis virus (TMEV) belongs to the genus Cardiovirus of the family Picornaviridae and is divided into two subgroups on the basis of different biological activities. GDVII subgroup strains produce acute and fatal polioencephalomyelitis in mice with no virus persistence. In contrast, DA or TO subgroup strains cause an early nonfatal polioencephalomyelitis. TMEV is thought to be an excellent animal model for the human demyelinating disease, multiple sclerosis. Data suggest that macrophages are a major reservoir harboring the virus. A small out-of-frame protein designated L* is synthesized in DA subgroup strains from an alternative, out-of-frame, initiation site. Studies of a DA mutant virus, having an ACG rather than an AUG and therefore does not synthesize L* protein, demonstrate that this protein is important for virus growth in particular cell types and is critical for DA-induced demyelinating disease and virus persistence. In addition, TMEV can be used as a vector for delivering foreign sequences into the central nervous system.
机译:泰勒氏鼠脑脊髓炎病毒(TMEV)属于Picornaviridae家族的心脏病毒属,根据不同的生物学活性分为两个亚组。 GDVII亚组株在没有病毒持久性的小鼠中产生急性和致命性脊髓灰质炎。相比之下,DA或TO亚组毒株会引起早期的非致命性脊髓灰质脑脊髓炎。 TMEV被认为是人类脱髓鞘疾病,多发性硬化症的极好的动物模型。数据表明巨噬细胞是携带该病毒的主要水库。从替代的无框架起始位点在DA亚组菌株中合成了一种称为L *的无框架蛋白质。对具有ACG而非AUG并因此不合成L *蛋白的DA突变病毒的研究表明,该蛋白对于特定细胞类型中的病毒生长非常重要,并且对于DA诱导的脱髓鞘疾病和病毒持久性至关重要。此外,TMEV可用作将外来序列传递到中枢神经系统的载体。

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