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AKR小鼠逆转录病毒致淋巴瘤特性的差异

Differences in lymphomagenic properties of AKR mouse retroviruses.

作者信息

Hays E F, Levy J A

出版信息

Virology. 1984 Oct 15;138(1):49-57. doi: 10.1016/0042-6822(84)90146-6.

DOI:10.1016/0042-6822(84)90146-6
PMID:6093361
Abstract

Long-term studies on lymphomagenicity of several AKR mouse retroviruses have shown that the biologically cloned ecotropic SL3-3c virus is the most lymphomagenic of all viruses tested. This fact was demonstrated by lymphomagenicity in five mouse strains SJL, C3Hf/Bi, C3H/HeJ, CBA/H, and NFS, and lymphoma acceleration in AKR mice. The incidence was higher and latent periods shorter than that found with the other retroviruses tested (SL3-1c, SL3-2c, MCFc, and GMuLVc). In addition, it was the only retrovirus found to be highly oncogenic in the C3H/HeJ and CBA/H strains. Lack of lymphomagenicity of MCFc in CBA/H strain was shown to be due to a block in viral replication. Addition of nononcogenic Akv ecotropic virus did not affect this lack of oncogenicity. The lymphomas developing in CBA/H and SJL mice after neonatal inoculation of SL3-3c virus only produced lymphomagenic ecotropic virus. Thus, SL3-3c lymphomagenesis is most likely due solely to the action of that virus. These studies indicate that pure ecotropic AKR viruses can be highly leukemogenic.

摘要

对几种AKR小鼠逆转录病毒致淋巴瘤性的长期研究表明,生物学克隆的嗜亲性SL3-3c病毒是所有测试病毒中致淋巴瘤性最强的。这一事实在五种小鼠品系SJL、C3Hf/Bi、C3H/HeJ、CBA/H和NFS的淋巴瘤发生情况以及AKR小鼠的淋巴瘤加速情况中得到了证实。其发病率高于其他测试的逆转录病毒(SL3-1c、SL3-2c、MCFc和GMuLVc),潜伏期也更短。此外,它是唯一在C3H/HeJ和CBA/H品系中具有高度致癌性的逆转录病毒。已证明MCFc在CBA/H品系中缺乏致淋巴瘤性是由于病毒复制受阻。添加非致癌性的嗜亲性Akv病毒并不影响这种致癌性的缺乏。新生期接种SL3-3c病毒后,CBA/H和SJL小鼠发生的淋巴瘤仅产生致淋巴瘤性嗜亲性病毒。因此,SL3-3c致淋巴瘤作用很可能仅归因于该病毒的作用。这些研究表明,纯嗜亲性AKR病毒可具有高度致白血病性。

相似文献

1
Differences in lymphomagenic properties of AKR mouse retroviruses.AKR小鼠逆转录病毒致淋巴瘤特性的差异
Virology. 1984 Oct 15;138(1):49-57. doi: 10.1016/0042-6822(84)90146-6.
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Molecular cloning of a highly leukemogenic, ecotropic retrovirus from an AKR mouse.从一只AKR小鼠中克隆出一种具有高度致白血病性的亲嗜性逆转录病毒。
J Virol. 1982 Sep;43(3):943-51. doi: 10.1128/JVI.43.3.943-951.1982.

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