Abstract
In order to prevent new pathogen outbreaks and avoid possible new global health threats, it is important to study the mechanisms of microbial pathogenesis, screen new antiviral agents and test new vaccines using the best methods. In the last decade, organoids have provided a groundbreaking opportunity for modeling pathogen infections in human brains, including Zika virus (ZIKV) infection. ZIKV is a member of the Flavivirus genus, and it is recognized as an emerging infectious agent and a serious threat to global health. Organoids are 3D complex cellular models that offer an in-scale organ that is physiologically alike to the original one, useful for exploring the mechanisms behind pathogens infection; additionally, organoids integrate data generated in vitro with traditional tools and often support those obtained in vivo with animal model. In this mini-review the value of organoids for ZIKV research is examined and sustained by the most recent literature. Within a 3D viewpoint, tissue engineered models are proposed as future biological systems to help in deciphering pathogenic processes and evaluate preventive and therapeutic strategies against ZIKV. The next steps in this field constitute a challenge that may protect people and future generations from severe brain defects.
Highlights
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While few studies tried to understand the viral effect during pregnancy, others focused on zika virus (ZIKV) infection on adults and neonates, and few others explored its sexual transmission, which is unique within the Flavivirus genus
The most recent study showing the superiority of brain organoids in modeling ZIKV infections has uncovered virus-specific mechanisms by comparing ZIKV with another common virus causing newborn morbidity, such as herpes simple virus (HSV)
Summary
The zika virus (ZIKV) is a vector borne-flavivirus, with a single serotype, but two differentiated lineages: the East/West African and the Asian genotypes [1]. In July of the same year, ZIKV was associated with Guillain–Barré syndrome in adults; in October, the first link of microencephaly in newborns of infected mothers was reported This association was supported by in vivo studies where the virus infected neural progenitors and impaired the brain development [4]. A total of 86 countries and territories have reported evidence of mosquitotransmitted Zika infection and the current epidemic is caused by ZIKV from an Asian lineage [10] and there is no vaccine or approved small-molecule based drug to prevent or efficiently treat ZIKV infection It is well-known that Zika spreads similar to other arboviruses [11] and, as ZIKV and Dengue (DENV) viruses share the same arthropod vector, the extent and effects of the immunologic cross-reactivity are of great interest for the scientific community [12]. Most of MAbs tested to date have shown a weak response against ZIKV, which, again, could create the risk of developing ADE related to ZIKV infection [14,15]
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