Department of Biological Sciences, and Purdue Institute of Inflammation, Immunology and Infectious Disease, Purdue University, West Lafayette, Indiana, USA.
Department of Biological Sciences, and Purdue Institute of Inflammation, Immunology and Infectious Disease, Purdue University, West Lafayette, Indiana, USA
mBio. 2017 Jun 27;8(3):e00916-17. doi: 10.1128/mBio.00916-17.
Zika virus caught the world by surprise by its rapid spread and frightening disease outcomes. This major epidemic motivated many scientists to focus their attention on controlling this emerging pathogen. As many as 45 vaccine candidates are being developed, but progress in the antiviral arena has been slower. In a recent article (mBio 8:e00350-17, 2017, https://doi.org/10.1128/mBio.00350-17), Costa and colleagues showed that an FDA-approved drug used to treat Alzheimer's disease may moderate Zika virus-induced neuronal damage. This work is based on the premise that overstimulation of -methyl-d-aspartate receptors (NMDARs) may drive neurodegeneration and that this may be responsible for neuronal cell death associated with Zika virus infection of the central nervous system (CNS). Thus, blockage of the NMDAR channel activity with FDA-approved memantine or other antagonists may reduce neurological complications associated with Zika virus infection. Repurposing a preapproved drug and targeting the host represent intriguing strategies and yet require more analysis prior to moving into clinical trials.
寨卡病毒的迅速传播及其可怕的疾病后果令全世界猝不及防。这一重大疫情促使许多科学家将注意力集中在控制这种新出现的病原体上。目前正在开发多达 45 种疫苗候选物，但抗病毒领域的进展较为缓慢。在最近的一篇文章（mBio 8:e00350-17, 2017, https://doi.org/10.1128/mBio.00350-17）中，Costa 及其同事表明，一种用于治疗老年痴呆症的美国食品药品监督管理局（FDA）批准的药物可能可以减轻寨卡病毒引起的神经元损伤。这项工作基于以下前提：过度刺激-甲基-d-天冬氨酸受体（NMDARs）可能会导致神经退行性变，而这可能是寨卡病毒感染中枢神经系统（CNS）所导致的神经元细胞死亡的原因。因此，用 FDA 批准的美金刚或其他拮抗剂阻断 NMDAR 通道活性可能会降低与寨卡病毒感染相关的神经并发症。重新利用已批准的药物并针对宿主是一种很有吸引力的策略，但在进入临床试验之前，还需要进行更多的分析。
