Oxidative stress in Mayaro virus infection
Oxidative stress in Mayaro virus infection
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DOI：
10.1016/j.virusres.2017.04.017
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发表时间：
2017-05-15
期刊：
影响因子：
5
通讯作者：
de Brito Magalhaes, Cintia Lopes
中科院分区：
文献类型：
--
作者：
Camini, Fernanda Caetano;da Silva Caetano, Camila Carla;de Brito Magalhaes, Cintia Lopes
马亚罗病毒（MAYV）是一种被忽视的热带虫媒病毒，引起发热综合征，有时伴有失能性关节炎/关节痛。MAYV的发病机制尚未完全确定，并且已发现由活性氧（ROS）增加和/或抗氧化剂防御耗尽介导的氧化应激促成病毒性疾病的几个方面。为了研究MAYV是否在宿主细胞中诱导氧化应激，我们在感染后的不同时间点监测ROS产生、氧化应激标志物和抗氧化防御。我们的研究结果表明，MAYV诱导感染的HepG 2细胞中的氧化应激，所示的丙二醛（MDA）和蛋白质羰基水平的增加，并通过显着降低还原型谷胱甘肽（GSH/GSSG）的比率。一般来说，MAYV感染的HepG 2细胞也表现出抗氧化防御的增加。我们观察到超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性和总谷胱甘肽含量的增加。为了确定在其他细胞类型中是否发生类似的作用，我们评估了MAYV感染后J774细胞中的ROS、MDA和SOD活性水平。与我们在HepG 2细胞中观察到的相似，J774细胞在MAYV感染后表现出ROS、MDA和总SOD活性的增加。因此，由于细胞的氧化还原环境的影响，生产和清除的ROS，我们假设，ROS的过度生产是负责的氧化应激反应的MAYV感染，尽管在抗氧化状态的增加。这项研究是第一份关于MAYV感染过程中氧化应激参与的报告。总的来说，我们的数据揭示了暴露于MAYV后宿主细胞中的一些机制。
Mayaro virus (MAYV) is a neglected tropical arbovirus that causes a febrile syndrome that is sometimes accompanied by incapacitating arthritis/arthralgia. The pathogenesis of MAYV has not been completely defined and oxidative stress mediated by an increase in reactive oxygen species (ROS) and/or depletion of antioxidant defences has been found to contribute to several aspects of viral disease. To investigate whether MAYV induced oxidative stress in host cells, we monitored ROS production, oxidative stress markers and antioxidant defences at different time points after infection. Our results show that MAYV induced significant oxidative stress in infected HepG2 cells, as indicated by the increase of malondialdehyde (MDA) and protein carbonyl levels, and by a significant decrease of the reduced versus oxidized glutathione (GSH/GSSG) ratio. Generally, MAYV-infected HepG2 cells also showed an increase in antioxidant defences. We observed an increase in the superoxide dismutase (SOD) and catalase (CAT) activities and the total glutathione content. To determine whether similar effects occurred in other cell types, we evaluated the ROS, MDA and SOD activity levels in J774 cells after MAYV infection. Similar to our observations in HepG2 cells, the J774 cells showed an increase in ROS, MDA and total SOD activity following MAYV infection. Thus, since the cellular redox environment is influenced by the production and removal of ROS, we hypothesize that the overproduction of ROS was responsible for the oxidative stress in response to the MAYV infection despite the increase in the antioxidant status. This study is the first report on the involvement of oxidative stress during MAYV infection. Collectively, our data shed light on some mechanisms that are operational in host cells following exposure to MAYV.