IFITM Genes, Variants, and Their Roles in the Control and Pathogenesis of Viral Infections.
IFITM Genes, Variants, and Their Roles in the Control and Pathogenesis of Viral Infections.
复制标题
IFITM 基因、变异体及其在病毒感染控制和发病机制中的作用
DOI：
10.3389/fmicb.2018.03228
复制
发表时间：
2018
影响因子：
5.2
通讯作者：
Guo Ju Tao
中科院分区：
文献类型：
--
作者：
Zhao Xuesen;Li Jiarui;Winkler Cheryl A;An Ping;Guo Ju Tao
干扰素诱导的跨膜蛋白(IFITM)是一类定位于血浆和内膜的小分子蛋白。IFITM不仅通过阻断病毒被膜和细胞膜之间的膜融合来抑制病毒进入宿主细胞，而且还减少了感染性病毒粒子的产生或子代病毒粒子的感染性。不足为奇的是，一些病毒可以逃避IFITM的限制，甚至劫持抗病毒蛋白，以便于它们感染进入宿主细胞或促进病毒粒子的组装，推测是通过调节膜融合。与许多其他在微生物感染的选择压力下进化的宿主防御基因类似，IFITM基因在脊椎动物中的进化速度加快，在人类群体中发现了许多单核苷酸多态(SNPs)，其中一些与病毒感染(如甲型流感病毒)的严重程度和预后有关。在这里，我们回顾了基因变异对IFITM限制病毒感染的作用和潜在影响。需要继续进行研究，以破译IFITM和病毒之间复杂相互作用的分子机制，以努力确定它们在体内病毒感染背景下的病理生物学作用。
Interferon-induced transmembrane proteins (IFITMs) are a family of small proteins that localize in the plasma and endolysosomal membranes. IFITMs not only inhibit viral entry into host cells by interrupting the membrane fusion between viral envelope and cellular membranes, but also reduce the production of infectious virions or infectivity of progeny virions. Not surprisingly, some viruses can evade the restriction of IFITMs and even hijack the antiviral proteins to facilitate their infectious entry into host cells or promote the assembly of virions, presumably by modulating membrane fusion. Similar to many other host defense genes that evolve under the selective pressure of microorganism infection, IFITM genes evolved in an accelerated speed in vertebrates and many single-nucleotide polymorphisms (SNPs) have been identified in the human population, some of which have been associated with severity and prognosis of viral infection (e.g., influenza A virus). Here, we review the function and potential impact of genetic variation for IFITM restriction of viral infections. Continuing research efforts are required to decipher the molecular mechanism underlying the complicated interaction among IFITMs and viruses in an effort to determine their pathobiological roles in the context of viral infections in vivo.