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AKR嗜亲性鼠白血病病毒SL3-3在体内形成包膜基因重组体。

AKR ecotropic murine leukemia virus SL3-3 forms envelope gene recombinants in vivo.

作者信息

Thomas C Y

出版信息

J Virol. 1986 Jul;59(1):23-30. doi: 10.1128/JVI.59.1.23-30.1986.

DOI:10.1128/JVI.59.1.23-30.1986
PMID:3012118
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC253033/
Abstract

The ecotropic AKR virus SL3-3 was injected into neonatal mice of the high-leukemia strains HRS/J and CWD/J and the low-leukemia strains CBA/J, SEA/J, and NIH Swiss. SL3-3 was highly leukemogenic in each strain, and 90% of the inoculated animals died by 6 months of age. T1 oligonucleotide fingerprint analysis of the genomic RNAs of viruses recovered from 9 of 13 leukemic animals revealed the presence of the SL3-3 virus and recombinant viruses with polytropic virus-related envelope gene sequences. Recombinant proviruses were detected by the Southern blot technique in the DNAs of 17 of 18 tumors. The pattern of substitutions within the envelope genes of the SL3-3 recombinant viruses appeared to be dependent on the strain of the animal. These observations indicate that the SL3-3 virus formed envelope gene recombinants in vivo in each of the strains that were studied. However, the role of these recombinants during leukemogenesis remains to be defined.

摘要

将亲嗜性AKR病毒SL3-3注射到高白血病品系HRS/J和CWD/J以及低白血病品系CBA/J、SEA/J和NIH瑞士小鼠的新生小鼠体内。SL3-3在每个品系中都具有高度致白血病性，90%的接种动物在6个月龄时死亡。对13只白血病动物中的9只所回收病毒的基因组RNA进行的T1寡核苷酸指纹分析显示，存在SL3-3病毒以及带有嗜异性病毒相关包膜基因序列的重组病毒。通过Southern印迹技术在18个肿瘤中的17个肿瘤的DNA中检测到了重组前病毒。SL3-3重组病毒包膜基因内的替换模式似乎取决于动物的品系。这些观察结果表明，SL3-3病毒在每个被研究的品系体内形成了包膜基因重组体。然而，这些重组体在白血病发生过程中的作用仍有待确定。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/98d525a845d4/jvirol00106-0037-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/04df7b7ddedc/jvirol00106-0032-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/ca9cbb06439d/jvirol00106-0033-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/f92ca3f763c8/jvirol00106-0034-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/d6ef87740c90/jvirol00106-0035-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/41d726eef5df/jvirol00106-0036-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/3b47f7588243/jvirol00106-0036-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/98d525a845d4/jvirol00106-0037-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/04df7b7ddedc/jvirol00106-0032-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/ca9cbb06439d/jvirol00106-0033-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/f92ca3f763c8/jvirol00106-0034-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/d6ef87740c90/jvirol00106-0035-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/41d726eef5df/jvirol00106-0036-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/3b47f7588243/jvirol00106-0036-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10ef/253033/98d525a845d4/jvirol00106-0037-a.jpg

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本文引用的文献

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Expression of leukemogenic recombinant viruses associated with a recessive gene in HRS/J mice.与隐性基因相关的致白血病重组病毒在HRS/J小鼠中的表达。
J Exp Med. 1980 Aug 1;152(2):249-64. doi: 10.1084/jem.152.2.249.
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Conformation of free and of integrated Moloney leukemia virus proviral DNA in preleukemic and leukemic BALB/Mo mice.前白血病和白血病BALB/Mo小鼠中游离及整合的莫洛尼白血病病毒前病毒DNA的构象
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在增强子中的核因子1位点发生突变后，鼠白血病病毒SL3-3对骨硬化症的诱导作用增强，但对淋巴瘤发生的影响未改变。
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Stability of AML1 (core) site enhancer mutations in T lymphomas induced by attenuated SL3-3 murine leukemia virus mutants.减毒SL3-3小鼠白血病病毒突变体诱导的T淋巴瘤中AML1（核心）位点增强子突变的稳定性
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