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用紫外线灭活流感病毒进行标记拯救

Marker rescue with ultraviolet-inactivated influenza virus.

作者信息

Sugiura A, Ueda M

出版信息

J Virol. 1971 Apr;7(4):499-503. doi: 10.1128/JVI.7.4.499-503.1971.

DOI:10.1128/JVI.7.4.499-503.1971
PMID:4939387
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC356150/
Abstract

Influenza Al/CAM virus undergoes abortive growth in FL cells, whereas X-3311, a recombinant virus clone from the cross between CAM and NWS, is capable of complete replication in FL cells and plaque formation on FL monolayers (FL-marker). Clone 1-5C-4 cells are permissive for both viruses. When either clone 1-5C-4 or FL cells, which were mixedly infected with both ultraviolet-irradiated X-3311 and active CAM viruses, were plated on FL monolayers, infective centers far exceeding in number those expected from the surviving X-3311 virus were observed, i.e., the FL-marker of the irradiated parent was rescued. The significantly lower radiation sensitivity of FL-marker than that of infectivity indicates that only part of the genome is responsible for the FL-marker. The capability of X-3311 virus to produce NP antigen and its infectivity were lost at the same time when the former was assayed under the condition of low multiplicity of infection. This suggests that only infectious virus is capable of producing NP antigen and that no stepwise inactivation of the viral genome occurs. It is also suggested that any lethal ultraviolet damage inflicted upon the viral genome prevents the expression of the portion of the genome coding for NP antigen.

摘要

甲型流感病毒/CAM病毒在FL细胞中生长受阻,而X - 3311是一种由CAM和NWS杂交产生的重组病毒克隆,它能够在FL细胞中完全复制并在FL单层细胞上形成蚀斑(FL标记)。克隆1 - 5C - 4细胞对这两种病毒均敏感。当用紫外线照射的X - 3311和活性CAM病毒混合感染克隆1 - 5C - 4细胞或FL细胞,并将其接种到FL单层细胞上时,观察到感染中心的数量远远超过了存活的X - 3311病毒预期的数量,即被照射亲本的FL标记被拯救。FL标记的辐射敏感性显著低于其感染性,这表明只有部分基因组负责FL标记。当在低感染复数条件下检测时,X - 3311病毒产生NP抗原的能力和其感染性同时丧失。这表明只有感染性病毒能够产生NP抗原,并且病毒基因组不会发生逐步失活。还表明病毒基因组受到的任何致死性紫外线损伤都会阻止编码NP抗原的基因组部分的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba23/356150/ef501e3b6d32/jvirol00280-0094-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba23/356150/ef501e3b6d32/jvirol00280-0094-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba23/356150/ef501e3b6d32/jvirol00280-0094-a.jpg

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本文引用的文献

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GENETIC STUDIES OF INFLUENZA VIRUSES. II. PLAQUE FORMATION BY INFLUENZA VIRUSES IN A CLONE OF A VARIANT HUMAN HETEROPLOID CELL LINE.流感病毒的遗传学研究。II. 流感病毒在一种变异人异倍体细胞系克隆中的蚀斑形成
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BEHAVIOR OF VIRUS-SPECIFIC ACTIVITIES IN TISSUE CULTURES INFECTED WITH MYXOVIRUSES AFTER CHEMICAL CHANGES OF THE VIRAL RIBONUCLEIC ACID.病毒核糖核酸发生化学变化后,感染黏液病毒的组织培养物中病毒特异性活性的表现
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Genetic recombination among influenza viruses. I. Cross reactivation of plaque-forming capacity as a method for selecting recombinants from the progeny of crosses between influenza A strains.
流感病毒间的基因重组。I. 蚀斑形成能力的交叉复活作为从甲型流感病毒株杂交后代中筛选重组体的一种方法。
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Genetic studies of influenza viruses. 3. Production of plaque-type recombinants with A0 and A1 strains.
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Genetic interaction between influenza A viruses of human and animal origin.甲型流感病毒在人类和动物来源毒株间的基因相互作用。
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