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细胞的体外淋巴细胞脉络丛脑膜炎病毒感染。

LCM virus infection of cells in vitro.

作者信息

Lehmann-Grube F, Popescu M, Schaefer H, Gschwender H H

出版信息

Bull World Health Organ. 1975;52(4-6):443-56.

PMID:1085205
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2366635/
Abstract

Most mammalian cells cultivated in vitro can be infected with lymphocytic choriomeningitis (LCM) virus. In addition to infectious virus, the cells produce antigenic material that fixes complement in the presence of antibody and is precipitated by antiserum. Intracellular antigen can also be demonstrated by the immunofluorescence procedure. When infected cells are viewed with the electron microscope, viral structures are seen either budding from or in association with the cell membranes. Immunoelectron microscopy, immunofluorescence, and cytotoxicity tests reveal virus-specific antigens on the surface of intact cells. Virus multiplication may be succeeded by cytolysis. Two LCM virus-specific antigens (or antigenic groups) can at present be distinguished. One corresponds to the infectious virus; the other is the complement-fixing "soluble" antigen. This extractable complement-fixing activity is produced by infected cells and is also a structural component of the infectious virus. It is not represented on the surface of either the virion or the infected cell. The cytolytic potential of LCM virus varies and is dependent on its previous passage history. Cytolytic and "attenuated" variants are able to initiate persistent infection of Mus musculus.Together with infectious virus, particles are produced that temporarily protect cells against standard virus. They appear to be by-products of virus multiplication, not in the sense of deletion mutants but of virus structures insufficiently equipped for their own active or passive replication, though capable of interfering with infectious virus. No evidence has been found for the generation of "defective interfering" particles, though their presence has not yet been excluded.

摘要

大多数体外培养的哺乳动物细胞可被淋巴细胞性脉络丛脑膜炎(LCM)病毒感染。除了感染性病毒外,细胞还产生抗原性物质,该物质在有抗体存在时能固定补体,并可被抗血清沉淀。细胞内抗原也可用免疫荧光法检测到。当用电子显微镜观察感染细胞时,可见病毒结构从细胞膜上芽生或与细胞膜相关联。免疫电子显微镜、免疫荧光和细胞毒性试验显示完整细胞表面存在病毒特异性抗原。病毒增殖之后可能继以细胞溶解。目前可区分两种LCM病毒特异性抗原(或抗原组)。一种与感染性病毒相对应;另一种是补体结合“可溶性”抗原。这种可提取的补体结合活性由感染细胞产生,也是感染性病毒的一种结构成分。它在病毒粒子或感染细胞的表面均未呈现。LCM病毒的细胞溶解潜力各不相同,取决于其先前的传代历史。细胞溶解和“减毒”变种能够引发小家鼠的持续性感染。与感染性病毒一起产生的粒子能暂时保护细胞免受标准病毒的侵害。它们似乎是病毒增殖的副产物,并非缺失突变体意义上的副产物,而是病毒结构不足以进行自身主动或被动复制,但能够干扰感染性病毒。尚未发现“缺陷干扰”粒子产生的证据,不过其存在尚未被排除。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/a20dc7108a44/bullwho00466-0068-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/5b99d9532c88/bullwho00466-0063-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/4231cd892623/bullwho00466-0064-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/f4ce7f564f52/bullwho00466-0065-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/f55b59a34767/bullwho00466-0066-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/6a6ff03fd043/bullwho00466-0067-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/a20dc7108a44/bullwho00466-0068-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/5b99d9532c88/bullwho00466-0063-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/4231cd892623/bullwho00466-0064-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/f4ce7f564f52/bullwho00466-0065-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/f55b59a34767/bullwho00466-0066-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/6a6ff03fd043/bullwho00466-0067-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ab/2366635/a20dc7108a44/bullwho00466-0068-a.jpg

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