Strating Jeroen Rpm, van Kuppeveld Frank Jm
Utrecht University, Faculty of Veterinary Medicine, Department of Infectious Diseases & Immunology, Division of Virology, Utrecht, The Netherlands.
Curr Opin Cell Biol. 2017 Aug;47:24-33. doi: 10.1016/j.ceb.2017.02.005. Epub 2017 Feb 24.
Positive-strand RNA (+RNA) viruses (e.g. poliovirus, hepatitis C virus, dengue virus, SARS-coronavirus) remodel cellular membranes to form so-called viral replication compartments (VRCs), which are the sites where viral RNA genome replication takes place. To induce VRC formation, these viruses extensively rewire lipid metabolism. Disparate viruses have many commonalities as well as disparities in their interactions with the host lipidome and accumulate specific sets of lipids (sterols, glycerophospholipids, sphingolipids) at their VRCs. Recent years have seen an upsurge in studies investigating the role of lipids in +RNA virus replication, in particular of sterols, and uncovered that membrane contact sites and lipid transfer proteins are hijacked by viruses and play pivotal roles in VRC formation.
正链RNA(+RNA)病毒(如脊髓灰质炎病毒、丙型肝炎病毒、登革热病毒、SARS冠状病毒)重塑细胞膜以形成所谓的病毒复制区室(VRC),病毒RNA基因组复制就在这些区域发生。为诱导VRC形成,这些病毒广泛重塑脂质代谢。不同的病毒在与宿主脂质组的相互作用方面既有许多共性也存在差异,并且在其VRC处积累特定的脂质组(固醇、甘油磷脂、鞘脂)。近年来,研究脂质在+RNA病毒复制中作用的研究激增,特别是对固醇的研究,并发现膜接触位点和脂质转运蛋白被病毒劫持,在VRC形成中起关键作用。