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HIV和仙台病毒导致的合胞体形成的温度增强作用。

Temperature enhancement of syncytium formation by HIV and Sendai virus.

作者信息

Kinchington D, Barker W, Galpin S, Apostolov K

机构信息

Department of Virology, Medical College of St. Bartholomew's Hospital, West Smithfield, London.

出版信息

J Med Virol. 1992 Jan;36(1):44-8. doi: 10.1002/jmv.1890360109.

Abstract

Syncytium formation, the characteristic cytopathic effect (CPE) of the human immunodeficiency virus (HIV) and cell fusion by Sendai virus, is accelerated by increasing the ambient temperature to values at which normal metabolic activity is inhibited. Uninfected C8166, CEM, and H9 cells were absorbed at 4 degrees C onto monolayers of H9 cells chronically infected with HIV and incubated subsequently at either 37 degrees C or 45 degrees C. Similarly chick and human erythrocytes and Hela cells were agglutinated with Sendai virus at 4 degrees C before incubation at temperatures of up to 50 degrees C. With both viruses the rate of cell fusion was directly related to temperature. Since membrane fluidity is dependent on the phase-transition temperature points of the membrane lipids it is proposed that sufficient membrane fluidity is essential for cell fusion to occur. The implication of these observations on the cytopathology of HIV is discussed.

摘要

多核体形成是人类免疫缺陷病毒(HIV)的特征性细胞病变效应(CPE)以及仙台病毒介导的细胞融合现象,当环境温度升高到抑制正常代谢活动的水平时,这种现象会加速。未感染的C8166、CEM和H9细胞在4℃下吸附到长期感染HIV的H9细胞单层上,随后分别在37℃或45℃下孵育。同样,鸡和人红细胞以及Hela细胞在4℃下与仙台病毒凝集,然后在高达50℃的温度下孵育。对于这两种病毒,细胞融合速率都与温度直接相关。由于膜流动性取决于膜脂的相变温度点,因此有人提出足够的膜流动性对于细胞融合的发生至关重要。本文讨论了这些观察结果对HIV细胞病理学的影响。

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