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麻疹病毒感染B淋巴细胞可使细胞活化,但会阻断细胞周期进程。

Measles virus infection of B lymphocytes permits cellular activation but blocks progression through the cell cycle.

作者信息

McChesney M B, Kehrl J H, Valsamakis A, Fauci A S, Oldstone M B

机构信息

Department of Immunology, Research Institute of Scripps Clinic, La Jolla, California 92037.

出版信息

J Virol. 1987 Nov;61(11):3441-7. doi: 10.1128/JVI.61.11.3441-3447.1987.

Abstract

Measles virus infection of unstimulated B lymphocytes suppresses both proliferation and differentiation into immunoglobulin-secreting cells. However, mitogenic stimulation of these infected cells results in cell volume enlargement, rapid RNA synthesis, and the expression of cell surface activation antigens 4F2, HLA-DS, and transferrin receptor. The cellular genes c-myc and histone 2B are induced during early G1 and S phase of the cell cycle, respectively, and viral RNA synthesis can be detected during this interval. However, total RNA synthesis is decreased at 48 h after stimulation, and the histone 2B RNA steady-state level at 48 h is fivefold less than that in uninfected cells. This sequence of events defines an arrest in the G1 phase of the cell cycle in measles virus-infected B cells.

摘要

未受刺激的B淋巴细胞感染麻疹病毒会抑制其增殖以及向分泌免疫球蛋白细胞的分化。然而,对这些受感染细胞进行促有丝分裂刺激会导致细胞体积增大、RNA快速合成以及细胞表面激活抗原4F2、HLA-DS和转铁蛋白受体的表达。细胞基因c-myc和组蛋白2B分别在细胞周期的G1早期和S期被诱导,并且在此期间可检测到病毒RNA合成。然而,刺激后48小时总RNA合成减少,且48小时时组蛋白2B RNA的稳态水平比未感染细胞低五倍。这一系列事件表明麻疹病毒感染的B细胞在细胞周期的G1期停滞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e22/255940/05534701659e/jvirol00102-0106-a.jpg

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