The role of microglia in Zika virus pathogenesis: Possible diagnostic and therapeutic strategies

The Zika virus, a member of the Flaviviridae family, is a mosquito-borne disease-causing virus that gained worldwide attention after a severe outbreak in Brazil in 2015. During this outbreak, some alarming evidence suggests that fetal microcephaly and other neuro-developmental disorders were associated with Zika infection. The virus also causes multi-organ failure and thrombocytopenia and also affects the eyes, leading to a potentially inflammatory disease called uveitis in adult individuals. It could be transmitted through sexual intercourse or the transplacental route, which is not commonly observed in other flaviviruses. In this review, we are interested in discovering the specific role of microglia in the pathogenesis of Zika virus-induced neuroinflammation. The virus comes into contact with microglial cells through the blood and causes activation and neuroinflammatory consequences, leading to the death of developing neurons and ultimately resulting in altered neuron-glia interaction. Despite its severity, there is still no specific medicine or vaccine available to combat the Zika infection. An essential aspect of this review is to identify cost-effective treatment strategies and accurate diagnostic methods for broader populations. In conclusion, an understanding of the cellular basis of Zika pathogenesis can help ensure potential treatment strategies to combat the global outbreak of the Zika virus. • ZIKV infection causes microcephaly and neuroinflammation in fetus. • ZIKV enters microglia via utilizing AXL, Tyro3 receptors. • The induction of TLR3 signaling promotes cytokine mediated neuroinflammation. • Activated microglia and astrocytes trigger abnormal neurogenesis or neuronal loss. • ZIKV can be treated with daptomycin, methacycline or NS2B-NS3 protease inhibitors.