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寨卡病毒发病机制中可能涉及的互补机制。

Complementary Mechanisms Potentially Involved in the Pathology of Zika Virus.

机构信息

Department of Immunology, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, United States.

Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, VA, United States.

出版信息

Front Immunol. 2018 Oct 15;9:2340. doi: 10.3389/fimmu.2018.02340. eCollection 2018.

DOI:10.3389/fimmu.2018.02340
PMID:30374352
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6196287/
Abstract

Zika virus (ZIKV) has emerged as a global health threat due to its neuro-teratogenic effect and wide range of transmission routes. Most recently, ZIKV infection has been linked with both autoimmune disorders in adults and neurodevelopmental disorders in newborns. Researchers are exploring potential cellular and molecular mechanisms underlying the neuro-teratogenicity and related consequences by using various cell culture methods and animal models. Though some of the putative viral entry receptors have been identified for ZIKV entry into the target cells, the exact mechanism of ZIKV entry or induced pathology are still not clear. Some of the important host cellular pathways including the toll-like receptor (TLR), autophagy, apoptosis and unfolded protein response (UPR) pathways are considered potential mechanism(s) for ZIKV induced neuroinflammation and for neurodevelopmental disorders. Since there is still a dire need for efficient treatment and vaccine to prevent ZIKV mediated disorders, a better understanding of the interaction between virus and host cellular pathways could pave the way for development of targeted therapeutic intervention. In this review, we are focusing on the recent advances and current knowledge regarding the interaction of ZIKV with abovementioned pathways so as to provide basic understanding to execute further research that could aid in the development of novel therapeutic strategy.

摘要

寨卡病毒(ZIKV)由于其神经致畸作用和广泛的传播途径,已成为全球健康威胁。最近,寨卡病毒感染与成人自身免疫性疾病和新生儿神经发育障碍有关。研究人员正在使用各种细胞培养方法和动物模型,探索寨卡病毒神经致畸性和相关后果的潜在细胞和分子机制。虽然已经确定了一些寨卡病毒进入靶细胞的假定病毒进入受体,但寨卡病毒进入或诱导病理的确切机制尚不清楚。一些重要的宿主细胞途径,包括 Toll 样受体(TLR)、自噬、细胞凋亡和未折叠蛋白反应(UPR)途径,被认为是寨卡病毒诱导的神经炎症和神经发育障碍的潜在机制。由于仍然迫切需要有效的治疗方法和疫苗来预防寨卡病毒介导的疾病,因此更好地了解病毒与宿主细胞途径之间的相互作用,可以为开发靶向治疗干预措施铺平道路。在这篇综述中,我们重点介绍了寨卡病毒与上述途径相互作用的最新进展和现有知识,以便为进一步研究提供基础理解,从而帮助开发新的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdad/6196287/3dc038921ffc/fimmu-09-02340-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdad/6196287/2f83f7f467ca/fimmu-09-02340-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdad/6196287/3dc038921ffc/fimmu-09-02340-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdad/6196287/2f83f7f467ca/fimmu-09-02340-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdad/6196287/3dc038921ffc/fimmu-09-02340-g0002.jpg

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