ZIKA VIRUS IMPAIRS NEUROBEHAVIORAL DEVELOPMENT AND INDUCES OXIDATIVE STRESS LINKED TO BLOOD–BRAIN BARRIER DISRUPTION IN A RAT MODEL OF CONGENITAL INFECTION

Аннотация

Zika virus (ZIKV) is an arbovirus belonging to the Flaviviridae family and the Flavivirus genus, which caused a significant epidemic in the Americas in 2015 (Song et al., 2017). Gestational ZIKV infection was soon linked to neurodevelopmental complications in fetuses, leading to various adverse outcomes such as intrauterine growth restriction, fetal death, miscarriage, stillbirth, and ocular abnormalities (Alvarado & Schwartz, 2017; Coyne & Lazear, 2016). Among these, microcephaly emerged as the most prominent clinical manifestation and is now well-established as a consequence of ZIKV vertical transmission (Wang & Ling, 2016; Li et al., 2016). While microcephaly was initially considered the primary neurological outcome of congenital ZIKV infection, recent studies have demonstrated that children affected by ZIKV in utero, even without microcephaly, may still exhibit neurodevelopmental delays (Sobral da Silva et al., 2021). Furthermore, growing evidence suggests that ZIKV-induced pathogenesis extends beyond the immediate postnatal period, with potential long-term effects on neurological development.