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

Abstract

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.

Keywords:

• ZIKV
• microcephaly
• neuroinflammatory response
• cell death

Funding

This work was supported by the Ministry of Science, Technology and Innovation/National Council for Scientific and Technological Development CNPQ/Brazil (grant numbers: 303999/2016-0, 439971/2016-0, and 440405/2016-5), and CAPES (Zika Fast-track).

Author contributions

All authors contributed towards data analysis, drafting and critically revising the paper, gave final approval of the version to be published, and agreed to be accountable for all aspects of the work.

Disclosure

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.