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

Abstract

Jorge Rodrigues de Sousa,1,2 Raimunda do Socorro da Silva Azevedo,1 Juarez Antônio Simões Quaresma,2–4 Pedro Fernando da Costa Vasconcelos1,4 1Departamento de Arbovirologia e Febres Hemorrágicas, Instituto Evandro Chagas, Ananindeua, Pará, Brazil; 2Núcleo de Medicina Tropical Belém, Universidade Federal do Pará, Belém, Pará, Brazil; 3Departamento de Patologia, Instituto Evandro Chagas, Ananindeua, Pará, Brazil; 4Universidade do Estado do Pará, Belém, Pará, BrazilCorrespondence: Pedro Fernando da Costa VasconcelosEvandro Chagas Institute, Rodovia BR-316, km-07, s/n, Ananindeua 67030-000, BrazilEmail [email protected]: 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

Keywords

• ZIKV
• microcephaly
• neuroinflammatory response
• cell death.