Zika Fetal Neuropathogenesis: Etiology of a Viral Syndrome.
Zika Fetal Neuropathogenesis: Etiology of a Viral Syndrome.
复制标题
DOI：
10.1371/journal.pntd.0004877
复制
发表时间：
2016-08
影响因子：
3.8
通讯作者：
Malone R
中科院分区：
文献类型：
--
作者：
Klase ZA;Khakhina S;Schneider Ade B;Callahan MV;Glasspool-Malone J;Malone R
寨卡病毒在美洲的持续流行以及观察到的与胎儿异常（原发性小头畸形）和成人自身免疫病理学（格林-巴利综合征）的关联引起了人们对这种被忽视的病原体的关注。虽然最初的病例研究引起了人们对寨卡病毒爆发的极大兴趣，但更大规模的前瞻性流行病学和基础病毒学研究检查了寨卡病毒感染的机制和相关的病理生理学，现在才开始发表。在这篇综述中，我们从比较病理学的角度分析了寨卡胎儿神经发病机制，使用“TORCH”病毒发病机制的历史隐喻提供背景。通过与其他胎儿病毒感染的相似之处，我们确定了共同的主题和机制，可能会阐明所观察到的病理。总结了各种细胞对寨卡病毒和其他黄病毒感染的易感性的现有数据。最后，我们强调黄病毒复制的已知分子机制的相关方面。
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.