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1型人类免疫缺陷病毒整合了糖基磷脂酰肌醇锚定的CD55和CD59以及整合膜蛋白CD46,其整合水平可保护病毒免受补体介导的破坏。

Human immunodeficiency virus type 1 incorporates both glycosyl phosphatidylinositol-anchored CD55 and CD59 and integral membrane CD46 at levels that protect from complement-mediated destruction.

作者信息

Saifuddin M, Hedayati T, Atkinson J P, Holguin M H, Parker C J, Spear G T

机构信息

Department of Immunology/Microbiology, Rush University, Chicago, IL 60612, USA.

出版信息

J Gen Virol. 1997 Aug;78 ( Pt 8):1907-11. doi: 10.1099/0022-1317-78-8-1907.

Abstract

Human immunodeficiency virus type 1 (HIV-1) can be either resistant or sensitive to complement-mediated destruction depending on the host cells. Incorporation of different levels of host cell CD46, CD55 and CD59 may account for this differential sensitivity to complement. However, it has not been determined whether CD46, CD55 and CD59 can all be incorporated at levels which protect virions. To determine whether each of these proteins can protect HIV-1, virions were derived from CHO cells expressing either human CD46, CD55 or CD59. Virions were shown to incorporate both glycosyl phosphatidylinositol (GPI)-anchored CD55 and CD59 as well as transmembrane CD46. Importantly, all three virus preparations were significantly more resistant to complement lysis than control virus. This study demonstrates that HIV-1 incorporates both transmembrane and GPI-anchored complement control proteins from host cells and that both types of protein increase complement resistance of virus.

摘要

1型人类免疫缺陷病毒(HIV-1)对补体介导的破坏作用可能具有抗性或敏感性,这取决于宿主细胞。宿主细胞中不同水平的CD46、CD55和CD59的掺入可能是造成这种对补体不同敏感性的原因。然而,尚未确定CD46、CD55和CD59是否都能以保护病毒粒子的水平掺入。为了确定这些蛋白质中的每一种是否能保护HIV-1,病毒粒子来源于表达人CD46、CD55或CD59的CHO细胞。结果表明,病毒粒子既能掺入糖基磷脂酰肌醇(GPI)锚定的CD55和CD59,也能掺入跨膜的CD46。重要的是,所有三种病毒制剂对补体裂解的抗性都明显高于对照病毒。这项研究表明,HIV-1从宿主细胞中掺入跨膜和GPI锚定的补体控制蛋白,并且这两种类型的蛋白都增加了病毒对补体的抗性。

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