Abstract

Zika virus (ZIKV) represents a public health challenge to Brazil and the rest of the world, especially because ZIKV infection has been linked to neurological sequelae, such as congenital fetal syndrome. Here, we aim 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 infection of different human cells in vitro.

Highlights

  • The Zika Virus (ZIKV) is an arbovirus of the genus Flavivirus, transmitted through the bite of the Aedes aegypti mosquito, and it became a public health problem[1]

  • It is far from clear all the mechanisms involved in the infection and how the ZIKV is able to cross barriers formed by endothelial cells (ECs), it has been shown that TAM receptors, especially Axl, act as a facilitator for the entry of the virus when it associates with the endogenous ligand Gas[6] (Growth arrest-specific 6)[2]

  • Until now we observed an increase of the Gas 6 levels in the serum of patients infected by ZIKV (Figure 1)

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Summary

Introduction

The Zika Virus (ZIKV) is an arbovirus of the genus Flavivirus, transmitted through the bite of the Aedes aegypti mosquito, and it became a public health problem[1]. Introduction The Zika Virus (ZIKV) is an arbovirus of the genus Flavivirus, transmitted through the bite of the Aedes aegypti mosquito, and it became a public health problem[1]. In the Americas, there have been over 200.000 confirmed cases of Zika fever (ZF), 60% of those in Brazil alone[1].

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