Programa de Pós Graduação em Ciências Biológicas, Núcleo de Pesquisas em Ciências Biológicas, NUPEB, Universidade Federal de Ouro Preto, Ouro Preto, Minas Gerais, Brazil.
Programa de Pós Graduação em Biotecnologia, Núcleo de Pesquisas em Ciências Biológicas, NUPEB, Universidade Federal de Ouro Preto, Ouro Preto, Minas Gerais, Brazil.
Virus Res. 2020 Sep;286:198084. doi: 10.1016/j.virusres.2020.198084. Epub 2020 Jul 2.
The first outbreak of Zika virus (ZIKV) infection in the Americas, especially in Brazil, was reported in 2015. Fever, headache, rash, and conjunctivitis are the common symptoms of ZIKV infection. Unexpected clinical outcomes, such as microcephaly and Guillain-Barré syndrome, have also been reported. The recent spread of ZIKV and its association with severe illness has created an urgent need to understand its pathogenesis and find potential therapeutic targets. Studies show that some viruses, including Flavivirus, trigger oxidative stress, which affects cellular metabolism, viral cycle, and pathogenesis. However, the role of oxidative stress in ZIKV infection needs to be investigated. Here, we analyzed ZIKV infection-triggered oxidative stress and modified antioxidant enzyme activities. U87-MG and HepG2 cells were infected to measure reactive oxygen species (ROS), malondialdehyde (MDA), and carbonyl protein levels, the activities of superoxide dismutase (SOD) and catalase (CAT), and the activation of nuclear factor erythroid 2p45-related factor 2 (Nrf2). ZIKV infection induced a significant increase in ROS, lipid peroxidation, and protein carbonylation products and a significant decrease in SOD and CAT activities accompanied by inhibition of Nrf2 activation in both cell lines. Further, MDA and carbonyl protein levels and SOD and CAT activities were evaluated in the brain and liver of ZIKV-infected C57BL/6 mice, and oxidative stress associated with antioxidant depletion was also found to occur in vivo. Together, our findings indicate the potential use of antioxidants as a novel therapeutic approach to Zika disease, and future studies in this direction are warranted.
寨卡病毒（ZIKV）于 2015 年首次在美洲爆发，尤其是在巴西。寨卡病毒感染的常见症状有发热、头痛、皮疹和结膜炎。此外，还报道了一些意外的临床结果，如小头畸形和格林-巴利综合征。寨卡病毒的近期传播及其与严重疾病的关联，促使人们迫切需要了解其发病机制并寻找潜在的治疗靶点。研究表明，包括黄病毒在内的一些病毒会引发氧化应激，从而影响细胞代谢、病毒周期和发病机制。然而，氧化应激在寨卡病毒感染中的作用仍需进一步研究。在这里，我们分析了寨卡病毒感染引发的氧化应激和抗氧化酶活性的改变。我们用 U87-MG 和 HepG2 细胞进行感染实验，以测量活性氧（ROS）、丙二醛（MDA）和羰基蛋白水平、超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性以及核因子红细胞 2 相关因子 2（Nrf2）的激活情况。寨卡病毒感染会显著增加 U87-MG 和 HepG2 细胞中的 ROS、脂质过氧化和蛋白质羰基化产物，并显著降低 SOD 和 CAT 的活性，同时抑制 Nrf2 的激活。进一步，我们在感染寨卡病毒的 C57BL/6 小鼠的大脑和肝脏中评估 MDA 和羰基蛋白水平以及 SOD 和 CAT 活性，发现体内也存在与抗氧化剂耗竭相关的氧化应激。总之，我们的研究结果表明，抗氧化剂可能作为一种新的治疗寨卡病的方法，值得进一步研究。
