Molecular mechanisms of Zika fever in inducing birth defects: an update

Abstract Zika virus (ZIKV) is a reemerging arthropod-borne Flavivirus and it has become a major international public health problem following the large outbreaks during 2013–16. ZIKV poses a serious threat to human beings because of its rapid spread and association with adverse pregnancy and neonatal outcomes, including miscarriage, microcephaly, Guillain–Barre syndrome, and other serious brain abnormalities and birth defects indicative of a Congenital Zika Syndrome. Aedes spp. mosquitoes are the primary vectors of ZIKV transmission in humans and it can also be transmitted through maternal–fetal route, blood transfusion, and sexual practices. To date, there is no vaccine and antiviral drug available to prevent or treat ZIKV infection due to the poor understanding of ZIKV–host interactions and the mechanisms associated with the disease manifestations. In the present report, we summarize the recent progress that has been made to define the ZIKV-mediated cellular apoptotic and immune response evasion pathways and the plausible molecular mechanisms underlying ZIKV-associated neurological disorders and birth defects in the developing fetuses and newborn babies, respectively, using several independent in vitro and in vivo animal studies. Knowledge on these mechanisms may contribute to the development of early diagnostics and preventive/therapeutic interventions for the control of ZIKV.