Laboratório de Vírus, Instituto de Ciências Biológicas, Departamento de Microbiologia, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
Universidade Federal dos Vales do Jequitinhonha e Mucuri, Diamantina, Brazil.
J Virol. 2019 Jun 28;93(14). doi: 10.1128/JVI.00312-19. Print 2019 Jul 15.
Viruses depend on cells to replicate and can cause considerable damage to their hosts. However, hosts have developed a plethora of antiviral mechanisms to counterattack or prevent viral replication and to maintain homeostasis. Advantageous features are constantly being selected, affecting host-virus interactions and constituting a harsh race for supremacy in nature. Here, we describe a new antiviral mechanism unveiled by the interaction between a giant virus and its amoebal host. Faustovirus mariensis infects , a free-living amoeba, and induces cell lysis to disseminate into the environment. Once infected, the cells release a soluble factor that triggers the encystment of neighbor cells, preventing their infection. Remarkably, infected cells stimulated by the factor encyst and trap the viruses and viral factories inside cyst walls, which are no longer viable and cannot excyst. This unprecedented mechanism illustrates that a plethora of antiviral strategies remains to be discovered in nature. Understanding how viruses of microbes interact with its hosts is not only important from a basic scientific point of view but also for a better comprehension of the evolution of life. Studies involving large and giant viruses have revealed original and outstanding mechanisms concerning virus-host relationships. Here, we report a mechanism developed by , a free-living amoeba, to reduce Faustovirus mariensis dissemination. Once infected, cells release a factor that induces the encystment of neighbor cells, preventing infection of further cells and/or trapping the viruses and viral factories inside the cyst walls. This phenomenon reinforces the need for more studies regarding large/giant viruses and their hosts.
病毒依赖细胞进行复制,会对宿主造成相当大的损害。然而,宿主已经发展出了大量的抗病毒机制来反击或阻止病毒复制,以维持体内平衡。有利的特征不断被选择,影响着宿主-病毒的相互作用,并构成了自然界中一场残酷的优胜劣汰的竞争。在这里,我们描述了一种由巨型病毒与其变形虫宿主相互作用揭示的新抗病毒机制。 Faustovirus mariensis 感染自由生活的变形虫,并诱导细胞裂解以传播到环境中。一旦被感染,细胞释放出一种可溶性因子,触发邻近细胞的包囊形成,从而阻止它们被感染。值得注意的是,受该因子刺激的感染细胞进行包囊,并将病毒和病毒工厂困在囊壁内,这些病毒和病毒工厂不再具有活力,也无法出囊。这种前所未有的机制表明,自然界中仍有大量的抗病毒策略有待发现。了解微生物的病毒与其宿主如何相互作用,不仅从基础科学的角度来看很重要,而且对于更好地理解生命的进化也很重要。涉及大型和巨型病毒的研究揭示了与病毒-宿主关系有关的原始和杰出机制。在这里,我们报告了一种由自由生活的变形虫 开发的机制,用于减少 Faustovirus mariensis 的传播。一旦被感染, 细胞释放出一种因子,诱导邻近细胞的包囊形成,阻止进一步的细胞感染和/或将病毒和病毒工厂困在囊壁内。这种现象强化了需要对大型/巨型病毒及其宿主进行更多研究的必要性。