Theiler's virus infection of 129Sv mice that lack the interferon alpha/beta or interferon gamma receptors.
Theiler's virus infection of 129Sv mice that lack the interferon alpha/beta or interferon gamma receptors.
复制标题
DOI：
10.1084/jem.181.6.2069
复制
发表时间：
1995-06-01
期刊：
影响因子：
--
通讯作者：
Bureau JF
中科院分区：
文献类型：
--
作者：
Fiette L;Aubert C;Müller U;Huang S;Aguet M;Brahic M;Bureau JF
泰勒病毒的丹尼尔斯株引起易感小鼠脊髓白色物质的持续感染，伴有慢性炎症和原发性脱髓鞘。近亲繁殖的129 Sv小鼠对这种感染有抵抗力;它们表现为轻度脑脊髓炎，并在几天内清除感染。一个非常不同的结果，观察到与近交系129 Sv小鼠，其受体的干扰素α/β或干扰素γ已被灭活的同源重组。前者表现为严重的脑脊髓炎，神经元急性感染，特别是在大脑和海马，广泛感染，脉络丛坏死。大多数动物死于这种急性疾病。后者表现出与对照129 Sv小鼠相同的早期脑脊髓炎。然而，他们仍然持续感染，并发展为非常严重的白色物质的晚期感染，伴有广泛的原发性脱髓鞘。这种晚期疾病看起来像是在易感近交系小鼠（如SJL/J或FVB品系）中观察到的慢性脱髓鞘疾病的加重形式。我们的研究结果表明，这两个干扰素系统在129 Sv小鼠抗泰勒病毒感染中起着非冗余的作用。他们还支持Ifg基因参与近交系小鼠对这种小核糖核酸病毒持续感染的抗性/易感性的观点。
The Daniels strain of Theiler's virus causes a persistent infection of the white matter of spinal cord of susceptible mice, with chronic inflammation and primary demyelination. Inbred 129Sv mice are resistant to this infection; they present with mild encephalomyelitis and clear the infection within a matter of days. A very different outcome was observed with inbred 129Sv mice whose receptors for interferon alpha/beta or interferon gamma had been inactivated by homologous recombination. The former presented severe encephalomyelitis with acute infection of neurons, particularly in brain and hippocampus, and extensive infection with necrosis of the choroid plexus. Most animals died of this acute disease. The latter, presented the same early encephalomyelitis as the control 129Sv mice. However, they remained persistently infected and developed a very severe late infection of the white matter with extensive primary demyelination. This late disease looked like an exacerbated form of the chronic demyelinating disease observed in susceptible inbred mice such as the SJL/J or FVB strains. Our results show that the two interferon systems play nonredundant roles in the resistance of the 129Sv mouse to the infection by Theiler's virus. They also lend support to the notion that the Ifg gene is involved in the resistance/susceptibility of inbred strains of mice to persistent infection by this picornavirus.