期刊
CELLULAR AND MOLECULAR LIFE SCIENCES
卷 78, 期 6, 页码 2485-2501出版社
SPRINGER BASEL AG
DOI: 10.1007/s00018-020-03711-8
关键词
Protein aggregation; Antiviral; Seeding; Surface-catalyzed nucleation
资金
- European Research Council under the European Union's Horizon 2020 Framework Programme ERC Grant [647458]
- Flanders institute for biotechnology (VIB)
- University of Leuven (Industrieel Onderzoeksfonds)
- Funds for Scientific Research Flanders (FWO) [G045920N, 1S48317N]
Research has shown that amyloids can encode important cellular functions, one of which involves interaction with microbial pathogens, including viruses. Amyloids expressed in humans can act as both innate restriction molecules against viruses and agents that promote viral infectivity. The underlying molecular driving forces of amyloid-virus interactions are not completely understood at present.
The aggregation of specific proteins and their amyloid deposition in affected tissue in disease has been studied for decades assuming a sole pathogenic role of amyloids. It is now clear that amyloids can also encode important cellular functions, one of which involves the interaction potential of amyloids with microbial pathogens, including viruses. Human expressed amyloids have been shown to act both as innate restriction molecules against viruses as well as promoting agents for viral infectivity. The underlying molecular driving forces of such amyloid-virus interactions are not completely understood. Starting from the well-described molecular mechanisms underlying amyloid formation, we here summarize three non-mutually exclusive hypotheses that have been proposed to drive amyloid-virus interactions. Viruses can indirectly drive amyloid depositions by affecting upstream molecular pathways or induce amyloid formation by a direct interaction with the viral surface or specific viral proteins. Finally, we highlight the potential of therapeutic interventions using the sequence specificity of amyloid interactions to drive viral interference.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据