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1型人类免疫缺陷病毒感染U937细胞可促进细胞分化及病毒组装的新途径。

Human immunodeficiency virus type 1 infection of U937 cells promotes cell differentiation and a new pathway of viral assembly.

作者信息

Pautrat G, Suzan M, Salaun D, Corbeau P, Allasia C, Morel G, Filippi P

机构信息

INSERM U322, Laboratoire des Rétrovirus et Maladies Associées, Marseille, France.

出版信息

Virology. 1990 Dec;179(2):749-58. doi: 10.1016/0042-6822(90)90142-e.

Abstract

The differentiation of U937 monoblastoid cells after human immunodeficiency virus type 1 (HIV-1) infection was studied using the following approaches: reverse transcriptase activity measurement, immunofluorescence labeling, and electron microscopy. For comparison, uninfected U937 cells were induced to differentiate from monocyte to macrophage by phorbol 12-myristate 13-acetate (PMA) or retinoic acid (RA) treatment. Both infected and drug-treated cells showed important and similar ultrastructural cell modifications, with a phenotype that decreased in monocyte specificity and increased in that of macrophages. When U937 cells were induced to differentiate upon HIV-1 infection, a very different pathway of viral production was observed. Production and accumulation of the virus in a vacuolar compartment of intracytoplasmic origin and escape to the antiviral lysosomal activity could explain virus persistence. This makes the cell system a good model with which to study the relationship between HIV-1 production and cell differentiation.

摘要

利用以下方法研究了1型人类免疫缺陷病毒(HIV-1)感染后U937单核母细胞样细胞的分化:逆转录酶活性测定、免疫荧光标记和电子显微镜检查。作为对照,用佛波酯12-肉豆蔻酸酯13-乙酸酯(PMA)或视黄酸(RA)处理未感染的U937细胞,诱导其从单核细胞分化为巨噬细胞。感染细胞和药物处理细胞均表现出重要且相似的超微结构细胞改变,其表型在单核细胞特异性方面降低,而在巨噬细胞特异性方面增加。当U937细胞因HIV-1感染而被诱导分化时,观察到一种非常不同的病毒产生途径。病毒在细胞质来源的液泡区室中产生和积累,并逃避抗病毒溶酶体活性,这可以解释病毒的持续存在。这使得该细胞系统成为研究HIV-1产生与细胞分化之间关系的良好模型。

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