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牛C型白血病病毒诱导多核巨细胞形成。

Induction of syncytia by the bovine C-type leukemia virus.

作者信息

Diglio C A, Ferrer J F

出版信息

Cancer Res. 1976 Mar;36(3):1056-67.

PMID:175949
Abstract

Bovine buffy coat cells infected with the bovine leukemia virus (BLV) induce syncytia formation in human diploid embryonic lung cells as well as in monolayer cell cultures of bovine, simian, ovine, bat, and caprine origin, but not in mouse fibroblast cells, normall rat kidney cells, or RSV-transformed rat cells. Syncytia were not observed in diploid embryonic lung cells inoculated with bovine buffy coat cells free of BLV. The syncytia-induction effect is associated with the synthesis of complete BLV by the buffy coat cells and is independent of whether these cells are viable, disrupted, normal, or malignant. Cell-free preparations of BLV and density gradient-purified virus also induce syncytia when added directly to diploid embryonic lung cells and to bovine, bat, and caprine monolayer cell cultures. Ether treatment, ultraviolet light irradiation, heating, freezing, and thawing destroy the syncytia-inducing activity of BLV. This activity is also neutralized when the virus is incubated with sera containing antibodies to BLV, but not when incubated with sera free of these antibodies or reference serum for the foamy-like bovine syncytial virus. Several other lines of evidence rule out the possibility that this virus or other bovine viruses are responsible for the syncytia-inducing phenomenon described here. BLV antigen was consistently detected by the immunofluorescent test in the syncytia-positive monolayer indicator cultures. However, syncytia formation was not necessarily associated with BLV production by the indicator cells. The ability to induce syncytia in monolayer cultures of nontransformed cells distinguishes BLV from all the known C-type luekemia viruses.

摘要

感染牛白血病病毒(BLV)的牛血沉棕黄层细胞可在人二倍体胚胎肺细胞以及牛、猴、羊、蝙蝠和山羊来源的单层细胞培养物中诱导多核巨细胞形成,但在小鼠成纤维细胞、正常大鼠肾细胞或劳氏肉瘤病毒(RSV)转化的大鼠细胞中则不会。接种不含BLV的牛血沉棕黄层细胞的二倍体胚胎肺细胞中未观察到多核巨细胞。多核巨细胞诱导效应与血沉棕黄层细胞合成完整的BLV有关,且与这些细胞是否存活、破裂、正常或恶性无关。将BLV的无细胞制剂和密度梯度纯化病毒直接添加到二倍体胚胎肺细胞以及牛、蝙蝠和山羊单层细胞培养物中时,也可诱导多核巨细胞形成。乙醚处理、紫外线照射、加热、冷冻和解冻会破坏BLV的多核巨细胞诱导活性。当病毒与含有抗BLV抗体的血清孵育时,这种活性也会被中和,但与不含这些抗体的血清或泡沫状牛多核巨细胞病毒的参考血清孵育时则不会。其他几条证据排除了这种病毒或其他牛病毒导致此处所述多核巨细胞诱导现象的可能性。通过免疫荧光试验在多核巨细胞阳性单层指示培养物中始终检测到BLV抗原。然而,多核巨细胞形成不一定与指示细胞产生BLV有关。在未转化细胞的单层培养物中诱导多核巨细胞形成的能力使BLV有别于所有已知的C型白血病病毒。

相似文献

1
Induction of syncytia by the bovine C-type leukemia virus.牛C型白血病病毒诱导多核巨细胞形成。
Cancer Res. 1976 Mar;36(3):1056-67.
2
In vitro transmission and propagation of the bovine leukemia virus in monolayer cell cultures.牛白血病病毒在单层细胞培养物中的体外传播与增殖
Cancer Res. 1976 Nov;36(11 Pt 1):4152-9.
3
Syncytia infectivity of assay of bovine leukemia virus.牛白血病病毒检测的合胞体感染性
Natl Inst Anim Health Q (Tokyo). 1982 Winter;22(4):147-53.
4
Use of a feline cell line in the syncytia infectivity assay for the detection of bovine leukemia virus infection in cattle.在用于检测牛白血病病毒感染的牛的多核体感染性试验中使用猫细胞系。
Am J Vet Res. 1981 Jan;42(1):9-14.
5
Cross-neutralization of ovine and bovine C-type leukemia virus-induced syncytia formation.绵羊和牛C型白血病病毒诱导的合胞体形成的交叉中和作用。
Cancer Res. 1977 May;37(5):1486-9.
6
Development of an in vitro infectivity assay for the C-type bovine leukemia virus.C型牛白血病病毒体外感染性检测方法的建立。
Cancer Res. 1976 Mar;36(3):1068-73.
7
A comparison of the bovine leukemia and bovine syncytial virus status in utero-tubal cells recovered from fluids used to flush the uterus and oviducts of BLV-infected, superovulated cattle.
Ann Rech Vet. 1988;19(1):19-26.
8
An infectivity assay for the bovine leukemia virus based on the induction of the major internal virion antigen in susceptible cell cultures.一种基于在易感细胞培养物中诱导主要内部病毒粒子抗原的牛白血病病毒感染性测定法。
Ann Rech Vet. 1978;9(4):729-34.
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An infectivity assay for bovine leukemia virus using the immunoperoxidase technique.一种使用免疫过氧化物酶技术的牛白血病病毒感染性测定法。
Cancer Res. 1979 Oct;39(10):3952-4.
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Comparison of four serologic tests for the detection of antibodies to bovine leukemia virus.用于检测牛白血病病毒抗体的四种血清学检测方法的比较。
Am J Vet Res. 1981 Jan;42(1):5-8.

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J Virol. 1984 Apr;50(1):267-70. doi: 10.1128/JVI.50.1.267-270.1984.
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Can J Comp Med. 1983 Jul;47(3):328-31.
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