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鉴定人类免疫缺陷病毒1型(HIV-1)vpu基因编码的一种蛋白质。

Identification of a protein encoded by the vpu gene of HIV-1.

作者信息

Cohen E A, Terwilliger E F, Sodroski J G, Haseltine W A

机构信息

Dana-Farber Cancer Institute, Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115.

出版信息

Nature. 1988 Aug 11;334(6182):532-4. doi: 10.1038/334532a0.

DOI:10.1038/334532a0
PMID:3043230
Abstract

Human immunodeficiency virus 1 (HIV-1) is the aetiological agent of AIDS. The virus establishes lytic, latent and non-cytopathic productive infection in cells in culture. The complexity of virus-host cell interaction is reflected in the complex organization of the viral genome. In addition to the genes that encode the virion capsid and envelope proteins and the enzymes required for proviral synthesis and integration common to all retroviruses, HIV-1 is known to encode at least four additional proteins that regulate virus replication, the tat, art, sor and 3' orf proteins, as well as a protein of unknown function from the open reading frame called R. Close examination of the nucleic acid sequences of the genomes of multiple HIV isolates raised the possibility that the virus encodes a previously undetected additional protein. Here we report that HIV-1 encodes a ninth protein and that antibodies to this protein are detected in the sera of people infected with HIV-1. This protein distinguishes HIV-1 isolates from the other human and simian immunodeficiency viruses (HIV-2 and SIV) that do not have the capacity to encode a similar protein.

摘要

人类免疫缺陷病毒1型(HIV-1)是艾滋病的病原体。该病毒在培养细胞中可建立裂解性、潜伏性和非细胞病变性生产性感染。病毒与宿主细胞相互作用的复杂性反映在病毒基因组的复杂组织中。除了编码病毒体衣壳和包膜蛋白以及所有逆转录病毒共有的前病毒合成和整合所需酶的基因外,已知HIV-1还编码至少四种调节病毒复制的额外蛋白,即反式激活因子(tat)、反式调节因子(art)、sor和3'开放阅读框蛋白,以及一个来自名为R的开放阅读框的功能未知蛋白。对多种HIV分离株基因组核酸序列的仔细检查提出了该病毒编码一种先前未检测到的额外蛋白的可能性。在此我们报告,HIV-1编码第九种蛋白,并且在感染HIV-1的人的血清中检测到针对该蛋白的抗体。这种蛋白将HIV-1分离株与其他没有能力编码类似蛋白的人类和猿猴免疫缺陷病毒(HIV-2和猴免疫缺陷病毒[SIV])区分开来。

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Identification of a protein encoded by the vpu gene of HIV-1.鉴定人类免疫缺陷病毒1型(HIV-1)vpu基因编码的一种蛋白质。
Nature. 1988 Aug 11;334(6182):532-4. doi: 10.1038/334532a0.
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