Abstract
The rapid spread of new outbreaks of human infection caused by Zika virus (ZIKV) has raised many global concerns since 2016. Despite the increasing knowledge of this virus, data on the pathogenesis of ZIKV are still missing. In particular, it is still unknown how the virus crosses the endothelial monolayer and gets access to the bloodstream. In the present work, we used human umbilical vein endothelial cells (HUVECs) as a model to study ZIKV infection in vitro. We demonstrated that HUVECs are an optimal reservoir for viral replication, as they were able to sustain ZIKV infection up to two weeks, without showing a cytopathic effect. In order to evaluate the integrity of endothelial monolayer, immunofluorescence was performed on mock-infected or ZIKV-infected cells ± peripheral blood mononuclear cells (PBMCs) or polymorphonuclear cells (PMN), 48 h p.i., by using an anti-VE-Cadherin antibody, a major adherence protein that maintains the integrity of intercellular junctions. In addition to infection, we noted that the presence of some components of the immune system, such as PMNs, played an important role in altering the endothelial monolayer in cell junctions, suggesting that presence at the site of infection probably promotes the spread of ZIKV in vivo in the bloodstream.
Highlights
Zika virus (ZIKV) is a re-emerging arthropod-borne virus belonging to the Flaviviridae family [1,2]
The virus was released from the apical surface of polarized human umbilical vein endothelial cells (HUVECs), but failed to alter their permeability, as it was already observed by others [15,25]
We found no significant difference in the permeability of the HUVEC monolayer among the ZIKV and mock-infected cells in a transwell system
Summary
Zika virus (ZIKV) is a re-emerging arthropod-borne virus (arbovirus) belonging to the Flaviviridae family [1,2]. Imported cases of Zika fever have been reported in travelers returning from areas with endemic/epidemic Zika fever, increasing the risk of virus dissemination where its vectors, such as Ae. aegypti and Ae. albopictus, are present This RNA virus is closely related to other members of the genus, including Dengue Virus (DENV), West Nile virus (WNV), Yellow Fever Virus (YFV), Tick-Borne Encephalitis Virus (TBEV), and Japanese Encephalitis Virus (JEV) [3]. Recent studies have demonstrated that fetal endothelial cells or human umbilical vein endothelial cells (HUVEC) are permissive for ZIKV infection, making HUVEC a key cell model for ZIKV studies [22] At present, it is unclear how ZIKV reaches immune-privileged sites within the body and breaches protective placental-fetal and blood-testis barriers, which leads to sexual transmission and congenital defects [23]. As monocytes can infiltrate many tissues, including immune-sheltered organs, they are ideal targets for infection [24]
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