Klase Zachary A, Khakhina Svetlana, Schneider Adriano De Bernardi, Callahan Michael V, Glasspool-Malone Jill, Malone Robert
Department of Biological Sciences, University of the Sciences, Philadelphia, Pennsylvania, United States of America.
Department of Bioinformatics and Genomics, University of North Carolina at Charlotte, Charlotte, North Carolina, United States of America.
PLoS Negl Trop Dis. 2016 Aug 25;10(8):e0004877. doi: 10.1371/journal.pntd.0004877. eCollection 2016 Aug.
The ongoing Zika virus epidemic in the Americas and the observed association with both fetal abnormalities (primary microcephaly) and adult autoimmune pathology (Guillain-Barré syndrome) has brought attention to this neglected pathogen. While initial case studies generated significant interest in the Zika virus outbreak, larger prospective epidemiology and basic virology studies examining the mechanisms of Zika viral infection and associated pathophysiology are only now starting to be published. In this review, we analyze Zika fetal neuropathogenesis from a comparative pathology perspective, using the historic metaphor of "TORCH" viral pathogenesis to provide context. By drawing parallels to other viral infections of the fetus, we identify common themes and mechanisms that may illuminate the observed pathology. The existing data on the susceptibility of various cells to both Zika and other flavivirus infections are summarized. Finally, we highlight relevant aspects of the known molecular mechanisms of flavivirus replication.
美洲地区持续爆发的寨卡病毒疫情,以及所观察到的该病毒与胎儿异常(主要是小头畸形)和成人自身免疫性病理状况(格林-巴利综合征)之间的关联,已使这种被忽视的病原体受到关注。虽然最初的病例研究引发了人们对寨卡病毒疫情的极大兴趣,但目前才开始发表规模更大的前瞻性流行病学研究以及基础病毒学研究,这些研究旨在探究寨卡病毒感染机制及相关病理生理学。在本综述中,我们从比较病理学角度分析寨卡病毒致胎儿神经病变的过程,运用“TORCH”病毒发病机制这一历史隐喻来提供背景信息。通过将其与其他胎儿病毒感染进行对比,我们找出可能阐明所观察到的病理状况的共同主题和机制。总结了关于各种细胞对寨卡病毒及其他黄病毒感染易感性的现有数据。最后,我们重点介绍黄病毒复制已知分子机制的相关方面。