Molecular Medicine Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.
Molecular Medicine Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA; Department of Biology, Johns Hopkins University, Baltimore, MD 21218, USA.
Biochim Biophys Acta Mol Cell Res. 2024 Jun;1871(5):119723. doi: 10.1016/j.bbamcr.2024.119723. Epub 2024 Apr 8.
Viruses have evolved complex mechanisms to exploit host factors for replication and assembly. In response, host cells have developed strategies to block viruses, engaging in a continuous co-evolutionary battle. This dynamic interaction often revolves around the competition for essential resources necessary for both host cell and virus replication. Notably, iron, required for the biosynthesis of several cofactors, including iron‑sulfur (FeS) clusters, represents a critical element in the ongoing competition for resources between infectious agents and host. Although several recent studies have identified FeS cofactors at the core of virus replication machineries, our understanding of their specific roles and the cellular processes responsible for their incorporation into viral proteins remains limited. This review aims to consolidate our current knowledge of viral components that have been characterized as FeS proteins and elucidate how viruses harness these versatile cofactors to their benefit. Its objective is also to propose that viruses may depend on incorporation of FeS cofactors more extensively than is currently known. This has the potential to revolutionize our understanding of viral replication, thereby carrying significant implications for the development of strategies to target infections.
病毒已经进化出复杂的机制来利用宿主因子进行复制和组装。作为回应，宿主细胞已经开发出策略来阻止病毒，从而参与到持续的共同进化斗争中。这种动态的相互作用通常围绕着争夺对宿主细胞和病毒复制都必不可少的关键资源展开。值得注意的是，铁是合成几种辅助因子（包括铁硫簇 (FeS)）所必需的，在传染病原体和宿主之间的资源竞争中，铁是一个关键元素。尽管最近有几项研究已经确定了 FeS 辅助因子是病毒复制机制的核心，但我们对它们在病毒蛋白中的具体作用以及负责将其纳入病毒蛋白的细胞过程的理解仍然有限。本综述旨在整合我们目前对被描述为 FeS 蛋白的病毒成分的认识，并阐明病毒如何利用这些多功能辅助因子来为自身谋利。其目的还在于提出病毒对 FeS 辅助因子的依赖可能比目前已知的更为广泛。这有可能彻底改变我们对病毒复制的理解，从而对制定靶向感染的策略产生重大影响。
