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细胞周期停滞的细胞的人类免疫缺陷病毒感染。

Human immunodeficiency virus infection of cells arrested in the cell cycle.

作者信息

Lewis P, Hensel M, Emerman M

机构信息

Department of Pediatrics, University of Washington, Seattle.

出版信息

EMBO J. 1992 Aug;11(8):3053-8. doi: 10.1002/j.1460-2075.1992.tb05376.x.

Abstract

Cell proliferation is necessary for proviral integration and productive infection of most retroviruses. Nevertheless, the human immunodeficiency virus (HIV) can infect non-dividing macrophages. This ability to grow in non-dividing cells is not specific to macrophages because, as we show here, CD4+ HeLa cells arrested at stage G2 of the cell cycle can be infected by HIV-1. Proliferation is necessary for these same cells to be infected by a murine retrovirus, MuLV. HIV-1 integrates into the arrested cell DNA and produces viral RNA and protein in a pattern similar to that in normal cells. In addition, our data suggest that the ability to infect non-dividing cells is due to one of the HIV-1 core virion proteins. HIV infection of non-dividing cells distinguishes lentiviruses from other retroviruses and is likely to be important in the natural history of HIV infection.

摘要

细胞增殖对于大多数逆转录病毒的前病毒整合和有效感染是必要的。然而,人类免疫缺陷病毒(HIV)能够感染非分裂的巨噬细胞。在非分裂细胞中生长的这种能力并非巨噬细胞所特有,因为正如我们在此所展示的,停滞在细胞周期G2期的CD4⁺ 海拉细胞能够被HIV-1感染。对于这些相同的细胞而言,增殖是被鼠逆转录病毒MuLV感染所必需的。HIV-1整合到停滞细胞的DNA中,并以与正常细胞相似的模式产生病毒RNA和蛋白质。此外,我们的数据表明,感染非分裂细胞的能力归因于HIV-1核心病毒粒子蛋白之一。HIV对非分裂细胞的感染使慢病毒有别于其他逆转录病毒,并且可能在HIV感染的自然病程中具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7380/556788/fb915c102be0/emboj00093-0284-a.jpg

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