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猿猴免疫缺陷病毒对人类CD4+细胞的选择性感染:与包膜糖蛋白诱导的融合相关的有效感染

Selective infection of human CD4+ cells by simian immunodeficiency virus: productive infection associated with envelope glycoprotein-induced fusion.

作者信息

Koenig S, Hirsch V M, Olmsted R A, Powell D, Maury W, Rabson A, Fauci A S, Purcell R H, Johnson P R

机构信息

Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.

出版信息

Proc Natl Acad Sci U S A. 1989 Apr;86(7):2443-7. doi: 10.1073/pnas.86.7.2443.

Abstract

Simian immunodeficiency virus (SIV) and human immunodeficiency virus share the property of tropism for CD4-bearing cells. Infection is initiated by a high-affinity interaction between CD4 and conserved domains on the viral envelope glycoprotein. In this report, we demonstrated that SIV had a restricted host range among human CD4+ cells when compared with human immunodeficiency virus type 1 or type 2. This restricted tropism was associated with the inability of the SIV envelope glycoprotein to induce membrane fusion in cells not susceptible to productive exogenous infection by SIV. We conclude that the major route of SIV entry into CD4+ cells is by envelope-mediated direct fusion with the cell and that additional envelope-cell interactions after CD4 binding are required for productive infection.

摘要

猴免疫缺陷病毒(SIV)和人类免疫缺陷病毒具有对表达CD4的细胞的嗜性。感染是由CD4与病毒包膜糖蛋白上保守结构域之间的高亲和力相互作用引发的。在本报告中,我们证明,与1型或2型人类免疫缺陷病毒相比,SIV在人类CD4 +细胞中的宿主范围有限。这种受限的嗜性与SIV包膜糖蛋白无法在不易受SIV进行性外源感染的细胞中诱导膜融合有关。我们得出结论,SIV进入CD4 +细胞的主要途径是通过包膜介导的与细胞直接融合,并且在CD4结合后还需要额外的包膜-细胞相互作用才能进行有效感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8517/286929/814dfe17c06d/pnas00247-0331-a.jpg

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