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SUN1 对 HIV-1 感染的核限制。

Nuclear restriction of HIV-1 infection by SUN1.

机构信息

Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.

Department of Virology, Virus & Immunity Unit, Institut Pasteur, Paris, France.

出版信息

Sci Rep. 2021 Sep 27;11(1):19128. doi: 10.1038/s41598-021-98541-4.

DOI:10.1038/s41598-021-98541-4
PMID:34580332
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8476499/
Abstract

Overexpression of the human Sad-1-Unc-84 homology protein 2 (SUN2) blocks HIV-1 infection in a capsid-dependent manner. In agreement, we showed that overexpression of SUN1 (Sad1 and UNC-84a) also blocks HIV-1 infection in a capsid-dependent manner. SUN2 and the related protein SUN1 are transmembrane proteins located in the inner membrane of the nuclear envelope. The N-terminal domains of SUN1/2 localizes to the nucleoplasm while the C-terminal domains are localized in the nuclear lamina. Because the N-terminal domains of SUN1/2 are located in the nucleoplasm, we hypothesized that SUN1/2 might be interacting with the HIV-1 replication complex in the nucleus leading to HIV-1 inhibition. Our results demonstrated that SUN1/2 interacts with the HIV-1 capsid, and in agreement with our hypothesis, the use of N-terminal deletion mutants showed that SUN1/2 proteins bind to the viral capsid by using its N-terminal domain. SUN1/2 deletion mutants correlated restriction of HIV-1 with capsid binding. Interestingly, the ability of SUN1/2 to restrict HIV-1 also correlated with perinuclear localization of these proteins. In agreement with the notion that SUN proteins interact with the HIV-1 capsid in the nucleus, we found that restriction of HIV-1 by overexpression of SUN proteins do not block the entry of the HIV-1 core into the nucleus. Our results showed that HIV-1 restriction is mediated by the interaction of SUN1/2N-terminal domains with the HIV-1 core in the nuclear compartment.

摘要

人源 Sad-1-Unc-84 同源蛋白 2（SUN2）的过表达以衣壳依赖性方式阻断 HIV-1 感染。一致地，我们表明 SUN1（Sad1 和 UNC-84a）的过表达也以衣壳依赖性方式阻断 HIV-1 感染。SUN2 和相关蛋白 SUN1 是位于核膜内膜的跨膜蛋白。SUN1/2 的 N 端结构域定位于核质，而 C 端结构域定位于核纤层。由于 SUN1/2 的 N 端结构域位于核质中，我们假设 SUN1/2 可能与细胞核内的 HIV-1 复制复合物相互作用，从而导致 HIV-1 抑制。我们的结果表明 SUN1/2 与 HIV-1 衣壳相互作用，并且与我们的假设一致，使用 N 端缺失突变体表明 SUN1/2 蛋白通过其 N 端结构域结合病毒衣壳。SUN1/2 缺失突变体与 HIV-1 衣壳结合的限制相关。有趣的是，SUN1/2 限制 HIV-1 的能力也与这些蛋白的核周定位相关。与 SUN 蛋白在细胞核中与 HIV-1 衣壳相互作用的观点一致，我们发现过表达 SUN 蛋白对 HIV-1 的限制并不阻止 HIV-1 核心进入细胞核。我们的结果表明，HIV-1 的限制是通过 SUN1/2N 端结构域与核内 HIV-1 核心的相互作用介导的。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/874a/8476499/053b8cb4c892/41598_2021_98541_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/874a/8476499/09c55ed525b6/41598_2021_98541_Fig8_HTML.jpg
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