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CD4免疫粘附分子,而非重组可溶性CD4,可阻断2型人类免疫缺陷病毒感染的淋巴细胞形成合胞体。

CD4 immunoadhesin, but not recombinant soluble CD4, blocks syncytium formation by human immunodeficiency virus type 2-infected lymphoid cells.

作者信息

Sekigawa I, Chamow S M, Groopman J E, Byrn R A

机构信息

Department of Medicine, New England Deaconess Hospital, Harvrd Medical School, Boston, Massachusetts 02215.

出版信息

J Virol. 1990 Oct;64(10):5194-8. doi: 10.1128/JVI.64.10.5194-5198.1990.

DOI:10.1128/JVI.64.10.5194-5198.1990
PMID:2398542
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC248017/
Abstract

Recombinant soluble CD4 (rCD4) has been shown to be an effective inhibitor of human immunodeficiency virus type 1 (HIV-1) and HIV-2 infection of lymphoid cells in vitro. In this report, we characterized the effects of rCD4, the V1V2 fragment of CD4, and the immunoadhesin CD4-immunoglobulin G on syncytium formation between lymphoid cells infected by HIV-1 or HIV-2 and uninfected cells. All three molecules blocked HIV-1-mediated syncytium formation, but only CD4-immunoglobulin G blocked HIV-2-mediated syncytium formation. rCD4 and the V1V2 fragment of CD4 enhanced HIV-2-mediated syncytium formation. These results suggest that the process of cell fusion is significantly different between HIV-1- and HIV-2-infected cells.

摘要

重组可溶性CD4(rCD4)已被证明是体外人免疫缺陷病毒1型(HIV-1)和HIV-2感染淋巴细胞的有效抑制剂。在本报告中,我们描述了rCD4、CD4的V1V2片段以及免疫粘附素CD4-免疫球蛋白G对HIV-1或HIV-2感染的淋巴细胞与未感染细胞之间合胞体形成的影响。所有这三种分子均能阻断HIV-1介导的合胞体形成,但只有CD4-免疫球蛋白G能阻断HIV-2介导的合胞体形成。rCD4和CD4的V1V2片段增强了HIV-2介导的合胞体形成。这些结果表明,HIV-1感染细胞和HIV-2感染细胞之间的细胞融合过程存在显著差异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7013/248017/a6532ac7788b/jvirol00065-0604-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7013/248017/14fbcb262e21/jvirol00065-0603-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7013/248017/a6532ac7788b/jvirol00065-0604-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7013/248017/14fbcb262e21/jvirol00065-0603-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7013/248017/a6532ac7788b/jvirol00065-0604-a.jpg

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