de Sousa Jorge Rodrigues, Azevedo Raimunda do Socorro da Silva, Quaresma Juarez Antônio Simões, Vasconcelos Pedro Fernando da Costa
Departamento de Arbovirologia e Febres Hemorrágicas, Instituto Evandro Chagas, Ananindeua, Pará, Brazil.
Núcleo de Medicina Tropical Belém, Universidade Federal do Pará, Belém, Pará, Brazil.
Infect Drug Resist. 2019 Sep 13;12:2917-2921. doi: 10.2147/IDR.S209213. eCollection 2019.
Zika virus (ZIKV) is an arbovirus that is transmitted by mosquitos. Its prototype was isolated in 1947 from serum of a sentinel Rhesus monkey () in the Zika forest of Uganda. As a member of the genus , family , ZIKV is enveloped and icosahedral and possesses a single-stranded, positive-sense RNA genome of approximately 10.7 kb. Epidemiologically, infection by ZIKV has become a global health concern in recent years because of the occurrence of epidemics, its speed of dissemination, routes of transmission, and the sequelae it can cause especially in newborns. At the neural level, there are still many gaps in our understanding of the mechanisms that induce ZIKV infection-associated microcephaly. However, some studies already demonstrated that underlying cell death is determinant to induce the congenital malformation. In this report, we reviewed the various mechanisms of cell injury involved in the immunopathogenesis of ZIKV infection and discussed its relationship with the death of neuronal and glial cells development and microcephaly.
寨卡病毒（ZIKV）是一种由蚊子传播的虫媒病毒。其原型于1947年从乌干达寨卡森林中一只哨兵恒河猴的血清中分离出来。作为黄病毒属、黄病毒科的成员，寨卡病毒具有包膜，呈二十面体，拥有一个约10.7kb的单链、正义RNA基因组。在流行病学方面，近年来寨卡病毒感染已成为全球健康问题，这是由于其疫情的发生、传播速度、传播途径以及它可能导致的后遗症，尤其是在新生儿中。在神经层面，我们对引发寨卡病毒感染相关小头畸形的机制的理解仍存在许多空白。然而，一些研究已经证明，潜在的细胞死亡是导致先天性畸形的决定性因素。在本报告中，我们回顾了寨卡病毒感染免疫发病机制中涉及的各种细胞损伤机制，并讨论了其与神经元和神经胶质细胞发育及小头畸形死亡的关系。
