Department of Immunology, Anhui Medical University, Hefei, Anhui Province 230032, China.
Future Microbiol. 2012 Sep;7(9):1117-26. doi: 10.2217/fmb.12.81.
Some intracellular/membranous factors exert intrinsic immunity against viral pathogens. Most recently, SAMHD1 has been shown to be one of these factors. SAMHD1 is a nucleus-localized protein, and mutations in the gene are associated with Aicardi-Goutières syndrome. As a triphosphohydrolase, it depletes the intracellular pool of dNTPs in myeloid cells, such as macrophages and dendritic cells, to a low level that establishes a precursor-deficient environment for the synthesis of lentiviral cDNA, thereby restricting viral replication in these host cells. However, some viruses evolve Vpx to recruit SAMHD1 onto the CRL4(DCAF1) E3 ubiquitin ligase in the cytoplasm for proteasome-dependent degradation, by which these viruses relieve SAMHD1-mediated restriction of primate lentivirus infection. In this review, we describe the latest knowledge of SAMHD1 biology.
一些细胞内/膜相关因子对病毒病原体发挥固有免疫作用。最近，SAMHD1 被证实为其中的一种因子。SAMHD1 是一种定位于细胞核的蛋白，其基因中的突变与 Aicardi-Goutières 综合征相关。作为三磷酸水解酶，它使髓系细胞（如巨噬细胞和树突状细胞）中的细胞内 dNTP 池耗尽至低水平，从而为合成慢病毒 cDNA 建立了前体缺乏的环境，从而限制了这些宿主细胞中的病毒复制。然而，一些病毒进化出 Vpx 蛋白，将 SAMHD1 募集到细胞质中的 CRL4（DCAF1）E3 泛素连接酶上，通过蛋白酶体依赖性降解，这些病毒解除了 SAMHD1 对灵长类慢病毒感染的限制。在这篇综述中，我们描述了 SAMHD1 生物学的最新知识。
