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[多瘤病毒的悖论。裂解感染还是肿瘤诱导?]

[The paradox of polyomaviruses. Lytic infection or tumor induction?].

作者信息

Sanjuan Norberto A

机构信息

Laboratorio de Patología Experimental, Departamento de Microbiología, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, 1121 Buenos Aires, Argentina.

出版信息

Medicina (B Aires). 2004;64(1):73-6.

Abstract

Murine polyomaviruses can produce lytic infections in mouse cell cultures or transform in vitro rat fibroblasts through a complex interaction with key cellular regulators. After infection of newborn mice, some strains of polyomavirus induce epithelial and mesenchymal tumors. It has been described that there is a direct relationship between viral dissemination in the mouse and tumor induction. However, at a single cell level lytic infection and transformation would not be able to coexist. The existence of 3 distinct cell populations in polyoma-induced tumors, classified according to the presence or absence of viral DNA and viral capsid protein VP-1 have been described. We have reported a fourth type of cell in the neoplasms, that can express the early and the late viral genes but do not allow virus assembly, probably due to underphosphorylation of VP-1. The mechanisms of polyoma intracellular migration and dissemination in the mouse are discussed, related to the virus' ability of tumor induction.

摘要

鼠多瘤病毒可在小鼠细胞培养物中产生裂解性感染,或通过与关键细胞调节因子的复杂相互作用在体外转化大鼠成纤维细胞。新生小鼠感染后,某些多瘤病毒株可诱发上皮和间充质肿瘤。已有描述表明,病毒在小鼠体内的传播与肿瘤诱发之间存在直接关系。然而,在单细胞水平上,裂解性感染和转化无法共存。多瘤病毒诱发的肿瘤中存在3种不同的细胞群体,根据病毒DNA和病毒衣壳蛋白VP-1的有无进行分类。我们报道了肿瘤中的第四种细胞类型,它可以表达病毒早期和晚期基因,但不允许病毒组装,这可能是由于VP-1磷酸化不足所致。本文讨论了多瘤病毒在小鼠体内的细胞内迁移和传播机制,及其与病毒诱发肿瘤能力的关系。

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