Coxsackievirus-induced chronic inflammatory myopathy: virus variants distinguish between acute cytopathic effects and pathogenesis of chronic disease.
Coxsackievirus-induced chronic inflammatory myopathy: virus variants distinguish between acute cytopathic effects and pathogenesis of chronic disease.
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柯萨奇病毒引起的慢性炎症性肌病：病毒变体区分急性细胞病变效应和慢性疾病的发病机制。
DOI：
10.1006/viro.1997.8592
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Messner,RP
中科院分区：
文献类型：
--
作者：
Tam,PE;Messner,RP
柯萨奇病毒B1图森株（CVB1T）感染可导致易感品系小鼠发生慢性炎性肌病（CIM）和后肢无力。在这项研究中，一组六个空斑纯化病毒表现出小或大的空斑表型，来自父母CVB1T和父母CVB1T已通过猴肾细胞传代。所有六种变异体在肌肉中引起类似的急性组织病理学，但四种传代病毒中的三种（AMP1、AMP2和AMP3）未诱导CIM，而第四种（MP3）引起一些后肢无力，但无相关的肌肉炎症。相反，直接从亲本CVB 1T原种分离的两种病毒（MP1和MP2）均为肌病性。大斑块MP2引起更高的死亡率和更迅速的抑制宿主细胞的生物合成，但MP1和MP2诱导CIM，这是由父母CVB1T诱导的。斑块大小是变异体的稳定特征，但与其诱导CIM的能力无关。六种变体中的五种在肌肉、猴肾细胞和G8成肌细胞中表现出相同的复制水平，而AMP3则选择性地复制受损。受体结合和病毒诱导的宿主细胞转录和翻译抑制与肌致病性无关。因此，大多数传代的变体是稳健的感染性病毒，表明CIM的病毒诱导并不仅仅取决于急性感染期间的致细胞病变性。
Infection with the Tucson strain of coxsackievirus B1 (CVB1T) causes the development of chronic inflammatory myopathy (CIM) and hind limb weakness in susceptible strains of mice. In this study, a panel of six plaque-purified viruses exhibiting either small or large plaque phenotypes was derived from parental CVB1Tand parental CVB1Tthat had been passaged through monkey kidney cells. All six variants caused similar acute histopathology in muscle, but three of four passaged viruses (AMP1, AMP2, and AMP3) did not induce CIM while the fourth (MP3) caused some hind limb weakness but without associated muscle inflammation. In contrast, both viruses (MP1 and MP2) isolated directly from the parental CVB1Tstock were myopathic. Large plaque MP2 caused higher mortality and more rapid inhibition of host cell biosynthesis, but both MP1 and MP2 induced CIM that was comparable to that induced by parental CVB1T. Plaque size was a stable characteristic of the variants but did not correlate with their ability to induce CIM. Five of the six variants showed equivalent levels of replication in muscle, monkey kidney cells, and G8 myoblasts while one, AMP3, was selectively impaired for replication. Receptor binding and virus-induced inhibition of host cell transcription and translation were not linked to myopathogenicity. Thus, most of the passaged variants are robust infectious viruses, suggesting that viral induction of CIM does not depend solely on cytopathogenicity during the acute infection.
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B 组柯萨奇病毒的流行病学
DOI：
10.1007/978-1-4757-0247-7_22
发表时间：
1988
期刊：
The Journal of Infectious Diseases
影响因子：
--
作者：
M. Pallansch
通讯作者：
M. Pallansch
通过聚合酶链反应检测病毒后疲劳综合征患者肌肉中的肠道病毒 RNA 序列。
影响因子：
--
作者：
J. Gow;W. Behan;G. Clements;C. Woodall;M. Riding;P. Behan
通讯作者：
P. Behan
病毒后疲劳综合征患者的慢性肠道病毒感染
DOI：
10.1016/s0140-6736(88)92722-5
发表时间：
1988
期刊：
The Lancet
影响因子：
--
作者：
G. Yousef;G. Mann;D. Smith;E. Bell;V. Murugesan;R. Mccartney;J. Mowbray
通讯作者：
J. Mowbray
柯萨奇病毒BI诱导的小鼠选择性多发性肌炎
DOI：
10.1093/infdis/140.2.239
发表时间：
1979
期刊：
The Journal of Infectious Diseases
影响因子：
--
作者：
C. Ray;L. Minnich;P. Johnson
通讯作者：
P. Johnson
DOI：
10.1016/s0022-2143(96)90029-3
发表时间：
1996-09
期刊：
The Journal of laboratory and clinical medicine
影响因子：
--
作者：
P. E. Tam;Ronald P. Messner
通讯作者：
P. E. Tam;Ronald P. Messner