Lipid droplets form complexes with viroplasms and are crucial for rotavirus replication.
Lipid droplets form complexes with viroplasms and are crucial for rotavirus replication.
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DOI：
10.1016/j.coviro.2016.05.008
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发表时间：
2016-08
影响因子：
5.9
通讯作者：
Desselberger, Ulrich
中科院分区：
文献类型：
--
作者：
Crawford, Sue E.;Desselberger, Ulrich
最近的证据表明，各种病原体的复制靶向细胞脂质代谢。脂滴是脂质稳态的主要贡献者，含有中性脂肪，但也被认为是参与信号转导、膜运输和免疫和炎症反应调节的动态细胞器。轮状病毒利用脂滴进行复制。轮状病毒的病毒颗粒是病毒RNA复制和未成熟颗粒组装的位点，在感染早期与细胞脂滴形成复合物。阻断脂肪酸合成或干扰脂滴稳态的化合物减少病毒质形成和感染性病毒后代的产量。脂滴对于轮状病毒以及黄病毒科的各种成员和几种细胞内细菌的复制至关重要。降低细胞内甘油三酯含量的化合物在动物模型中减少了轮状病毒的复制，并且应该被认为是针对由轮状病毒、黄病毒和细胞内细菌引起的疾病的潜在治疗剂。
Recent evidence has demonstrated that a variety of pathogens target cellular lipid metabolism for their replication. Lipid droplets are a major contributor to lipid homeostasis and contain neutral fats but are also recognized as dynamic organelles involved in signal transduction, membrane trafficking and modulation of immune and inflammatory responses. Rotaviruses co-opt lipid droplets for their replication. Rotavirus viroplasms, sites of viral RNA replication and immature particle assembly, form complexes with cellular lipid droplets early in infection. Chemical compounds blocking fatty acid synthesis or interfering with lipid droplet homeostasis decrease viroplasm formation and the yield of infectious viral progeny. Lipid droplets are vital for the replication of rotaviruses as well as various members of the Flaviviridae family and several intracellular bacteria. Chemical compounds decreasing intracellular triglyceride content reduced rotavirus replication in an animal model and should be considered as potential therapeutic agents against disease caused by rotaviruses, flaviviruses and intracellular bacteria.
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