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低剂量分次全身照射对感染弗氏病毒复合物小鼠中SFFV mRNA、基因组DNA和蛋白表达的影响。

Effect of split low dose total body irradiation on SFFV mRNA, genomic DNA and protein expression in mice infected with the Friend virus complex.

作者信息

Shen R N, Lu L, Harrington M A, Srivastava C, Kim Y J, Zhou S Z, Wu B, Ruscetti S, Broxmeyer H E

机构信息

Department of Medicine Hematology/Oncology, Indiana University School of Medicine, Indianapolis 46202-5121.

出版信息

Leukemia. 1991 Mar;5(3):225-9.

PMID:2013981
Abstract

DBA/2 mice infected with lethal dosages of Friend virus complex (FVC) can be 100% cured by split-dose total body irradiation (TBI) at 150 cGy, an effect associated with the restoration of the cellular immunity which is compromised by the virus. The exact mechanism underlying the curative effect is unknown, but it may involve the interferon (IFN) system and interleukin-2 (IL-2) production. Initial studies indicated that TBI did not directly inactivate the virus, suggesting that irradiation either acted on the target cells for virus replication or on other cells mediating the effect. We have now examined the effect of this relatively low dose TBI on replication, transcription, and protein expression of the Friend virus. Northern blot analysis revealed that in FVC infected mice treated with curative low dose TBI, no spleen focus-forming virus (SFFV)-specific mRNA species were detected. Southern blot analysis revealed that a 6.0 kb SFFV fragment could be detected in infected, untreated spleen cells, but not in cells from FVC-infected mice treated with TBI, or in uninfected spleen cells. Western blot analysis revealed that the SFFV envelope glycoprotein was expressed in the spleen cells from untreated FVC infected mice, but not in the cells from TBI treated FVC infected mice. These results, consistent with our previous findings of greatly reduced spleen focus forming units in mice with FVC which had been treated with this regimen of TBI, suggest the possibility of using such treatments in other retroviral associated disorders.

摘要

感染致死剂量弗瑞德病毒复合物(FVC)的DBA/2小鼠,通过150厘戈瑞的分次全身照射(TBI)可100%治愈,这一效应与受病毒损害的细胞免疫的恢复有关。治愈效果的具体机制尚不清楚,但可能涉及干扰素(IFN)系统和白细胞介素-2(IL-2)的产生。初步研究表明,TBI不会直接使病毒失活,这表明照射要么作用于病毒复制的靶细胞,要么作用于介导该效应的其他细胞。我们现在研究了这种相对低剂量TBI对弗瑞德病毒复制、转录和蛋白质表达的影响。Northern印迹分析显示,在用治愈性低剂量TBI治疗的FVC感染小鼠中,未检测到脾集落形成病毒(SFFV)特异性mRNA种类。Southern印迹分析显示,在未处理的感染脾细胞中可检测到一个6.0 kb的SFFV片段,但在用TBI治疗的FVC感染小鼠的细胞或未感染的脾细胞中未检测到。Western印迹分析显示,未处理的FVC感染小鼠的脾细胞中表达SFFV包膜糖蛋白,但在用TBI治疗的FVC感染小鼠的细胞中未表达。这些结果与我们之前的发现一致,即接受这种TBI方案治疗的FVC小鼠的脾集落形成单位大幅减少,提示了在其他逆转录病毒相关疾病中使用此类治疗方法的可能性。

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Effect of split low dose total body irradiation on SFFV mRNA, genomic DNA and protein expression in mice infected with the Friend virus complex.低剂量分次全身照射对感染弗氏病毒复合物小鼠中SFFV mRNA、基因组DNA和蛋白表达的影响。
Leukemia. 1991 Mar;5(3):225-9.
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Curative effect of split low dosage total-body irradiation on mice infected with the polycythemia-inducing strain of the Friend virus complex.分割低剂量全身照射对感染弗氏病毒复合体红细胞增多诱导株小鼠的疗效
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Influence of recombinant human interleukin (IL)-7 on disease progression in mice infected with Friend virus complex.重组人白细胞介素(IL)-7对感染弗氏病毒复合物小鼠疾病进展的影响。
Int J Cancer. 1992 Sep 9;52(2):261-5. doi: 10.1002/ijc.2910520218.

引用本文的文献

1
Friend leukemia virus infection enhances DNA damage-induced apoptosis of hematopoietic cells, causing lethal anemia in C3H hosts.Friend白血病病毒感染增强了DNA损伤诱导的造血细胞凋亡,导致C3H宿主发生致死性贫血。
J Virol. 2002 Aug;76(15):7790-8. doi: 10.1128/jvi.76.15.7790-7798.2002.