鞘脂
先天免疫系统
溶瘤病毒
生物
病毒复制
免疫系统
鞘氨醇
鞘氨醇激酶
干扰素
病毒学
细胞生物学
病毒
1-磷酸鞘氨醇
免疫学
受体
生物化学
作者
Judith Bezgovsek,Erich Gulbins,Sarah-Kim Friedrich,Karl S. Lang,Vikas Duhan
标识
DOI:10.1515/hsz-2018-0181
摘要
Abstract In this review, we summarize the mechanisms by which sphingolipids modulate virus multiplication and the host innate immune response, using a number of host-virus systems as illustrative models. Sphingolipids exert diverse functions, both at the level of the viral life cycle and in the regulation of antiviral immune responses. Sphingolipids may influence viral replication in three ways: by serving as (co)receptors during viral entry, by modulating virus replication, and by shaping the antiviral immune response. Several studies have demonstrated that sphingosine kinases (SphK) and their product, sphingosine-1-phosphate (S1P), enhance the replication of influenza, measles, and hepatitis B virus (HBV). In contrast, ceramides, particularly S1P and SphK1, influence the expression of type I interferon (IFN-I) by modulating upstream antiviral signaling and enhancing dendritic cell maturation, differentiation, and positioning in tissue. The synthetic molecule α-galactosylceramide has also been shown to stimulate natural killer cell activation and interferon (IFN)-γ secretion. However, to date, clinical trials have failed to demonstrate any clinical benefit for sphingolipids in the treatment of cancer or HBV infection. Taken together, these findings show that sphingolipids play an important and underappreciated role in the control of virus replication and the innate immune response.
科研通智能强力驱动
Strongly Powered by AbleSci AI