The Zika Virus (ZIKV) is an arbovirus of the genus Flavivirus, transmitted through the bite of the Aedes aegypti mosquito, which has recently become a public health problem. In the Americas there have been over 200.000 confirmed cases of Zika fever (ZF), with over 60% of those in Brazil alone. Although the infection is generally asymptomatic, recent data show the link between ZIKV infection to neurological sequelae, such as Guillan-Barré syndrome, encephalitis, and meningitis in adults, and to a congenital fetal syndrome that includes fetal microcephaly. Despite the fact that yet all the mechanisms involved in the infection, and how the ZIKV is able to cross barriers formed by endothelial cells (ECs) is unknown, it has been shown that, the TAM family receptors, especially Axl, act as a facilitator for the entry of the virus when it associates with Axl's endogenous ligand (GAS6) (growth arrest-specific 6). Therefore, this project aims to verify the role of Gas6 in the pathogenesis of ZIKV infection, by evaluating the expression of Gas6 and TAM receptors in patients infected by the virus with different degrees of disease severity, and in vitro infection of different human cells. These aims will provide a better understanding of the relationship of the GAS6/TAM receptor axis with the pathogenicity of ZIKV, which may have important therapeutic consequences.
News published in Agência FAPESP Newsletter about the scholarship: