Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.
Department of Molecular Virology, Tokyo Medical and Dental University, Tokyo, Japan.
Nat Med. 2015 Dec;21(12):1502-7. doi: 10.1038/nm.3956. Epub 2015 Nov 2.
Membrane-associated RING-CH 8 (MARCH8) is one of 11 members of the recently discovered MARCH family of RING (really interesting new gene)-finger E3 ubiquitin ligases. MARCH8 downregulates several host transmembrane proteins, including major histocompatibility complex (MHC)-II, CD86, interleukin (IL)-1 receptor accessory protein, TNF-related apoptosis-inducing ligand (TRAIL) receptor 1 and the transferrin receptor. However, its physiological roles remain largely unknown. Here we identify MARCH8 as a novel antiviral factor. The ectopic expression of MARCH8 in virus-producing cells does not affect levels of lentivirus production, but it does markedly reduce viral infectivity. MARCH8 blocks the incorporation of HIV-1 envelope glycoprotein into virus particles by downregulating it from the cell surface, probably through their interaction, resulting in a substantial reduction in the efficiency of viral entry. The inhibitory effect of MARCH8 on vesicular stomatitis virus G-glycoprotein is even more remarkable, suggesting a broad-spectrum inhibition of enveloped viruses by MARCH8. Notably, the endogenous expression of MARCH8 is high in monocyte-derived macrophages and dendritic cells, and MARCH8 knockdown or knockout in macrophages significantly increases the infectivity of virions produced by these cells. Our findings thus indicate that MARCH8 is highly expressed in terminally differentiated myeloid cells, and that it is a potent antiviral protein that targets viral envelope glycoproteins and reduces their incorporation into virions.
膜相关环指蛋白 8(MARCH8)是最近发现的 RING(真正有趣的新基因)-指 E3 泛素连接酶家族的 11 个成员之一。MARCH8 下调了几种宿主跨膜蛋白,包括主要组织相容性复合体(MHC)-II、CD86、白细胞介素(IL)-1 受体辅助蛋白、肿瘤坏死因子相关凋亡诱导配体(TRAIL)受体 1 和转铁蛋白受体。然而,其生理作用仍知之甚少。在这里,我们将 MARCH8 鉴定为一种新的抗病毒因子。在产生病毒的细胞中外源表达 MARCH8 不会影响慢病毒的产生水平,但会显著降低病毒的感染力。MARCH8 通过从细胞表面下调 HIV-1 包膜糖蛋白来阻止其掺入病毒颗粒,可能通过相互作用导致病毒进入效率大幅降低。MARCH8 对水疱性口炎病毒 G-糖蛋白的抑制作用甚至更为显著,表明 MARCH8 对包膜病毒具有广谱抑制作用。值得注意的是,MARCH8 在单核细胞衍生的巨噬细胞和树突状细胞中表达水平较高,而巨噬细胞中的 MARCH8 敲低或敲除显著增加了这些细胞产生的病毒粒子的感染力。我们的研究结果表明,MARCH8 在终末分化的髓样细胞中高度表达,是一种针对病毒包膜糖蛋白的有效抗病毒蛋白,可降低其掺入病毒颗粒的效率。