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Cell Death And Zika Virus: An Integrated Network Of The Mechanisms Of Cell Injury

机译:细胞死亡和寨卡病毒:细胞损伤机制的综合网络

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Zika virus (ZIKV) is an arbovirus that is transmitted by Aedes mosquitos. Its prototype was isolated in 1947 from serum of a sentinel Rhesus monkey ( Macaca mulatta ) in the Zika forest of Uganda. As a member of the genus Flavivirus , family Flaviviridae , 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.
机译:寨卡病毒(ZIKV)是一种蚊虫,由伊蚊(Aedes mosquitos)传播。其原型于1947年从乌干达Zika森林中的定点恒河猴(Macaca mulatta)的血清中分离出来。作为黄病毒属黄病毒科的成员,ZIKV被包裹并呈二十面体,并具有约10.7 kb的单链正链RNA基因组。在流行病学上,由于流行病的发生,传播速度,传播途径及其可能引起的后遗症,近年来ZIKV感染已成为全球卫生关注的问题。在神经水平上,我们对诱导ZIKV感染相关小头畸形的机制的理解仍然存在许多空白。但是,一些研究已经证明,潜在的细胞死亡是诱发先天性畸形的决定因素。在本报告中,我们综述了ZIKV感染免疫机制中涉及的细胞损伤的各种机制,并讨论了其与神经元和神经胶质细胞发育死亡以及小头畸形的关系。

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