Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC H3T 1E2, Canada.
Department of Microbiology & Immunology, McGill University, Montreal, QC H3A 2B4, Canada.
Viruses. 2018 Jan 13;10(1):36. doi: 10.3390/v10010036.
Viruses exploit the host and induce drastic metabolic changes to ensure an optimal environment for replication and the production of viral progenies. In response, the host has developed diverse countermeasures to sense and limit these alterations to combat viral infection. One such host mechanism is through interferon signaling. Interferons are cytokines that enhances the transcription of hundreds of interferon-stimulated genes (ISGs) whose products are key players in the innate immune response to viral infection. In addition to their direct targeting of viral components, interferons and ISGs exert profound effects on cellular metabolism. Recent studies have started to illuminate on the specific role of interferon in rewiring cellular metabolism to activate immune cells and limit viral infection. This review reflects on our current understanding of the complex networking that occurs between the virus and host at the interface of cellular metabolism, with a focus on the ISGs in particular, cholesterol-25-hydroxylase (CH25H), spermidine/spermine acetyltransferase 1 (SAT1), indoleamine-2,3-dioxygenase (IDO1) and sterile alpha motif and histidine/aspartic acid domain-containing protein 1 (SAMHD1), which were recently discovered to modulate specific metabolic events and consequently deter viral infection.
病毒利用宿主并诱导剧烈的代谢变化，以确保复制和产生病毒后代的最佳环境。作为回应，宿主已经开发出多种对策来感知和限制这些改变，以对抗病毒感染。宿主的一种机制是通过干扰素信号转导。干扰素是细胞因子，可增强数百种干扰素刺激基因（ISGs）的转录，这些基因的产物是抗病毒感染固有免疫反应的关键因素。除了直接靶向病毒成分外，干扰素和 ISGs 对细胞代谢产生深远影响。最近的研究开始阐明干扰素在重新连接细胞代谢以激活免疫细胞和限制病毒感染方面的特定作用。这篇综述反映了我们目前对病毒和宿主在细胞代谢界面处发生的复杂网络的理解，特别是特别关注 ISGs，胆固醇-25-羟化酶（CH25H）、亚精胺/精胺乙酰转移酶 1（SAT1）、吲哚胺 2,3-双加氧酶（IDO1）和无菌α基序和组氨酸/天冬氨酸域包含蛋白 1（SAMHD1），它们最近被发现调节特定的代谢事件，从而阻止病毒感染。
