Evaluation of the Expression of CCR5 and CX3CR1 Receptors and Correlation with the Functionality of T Cells in Women infected with ZIKV during Pregnancy.

There have been reports of neurological abnormalities associated with the Zika virus (ZIKV), such as congenital Zika syndrome (CZS) in children born to mothers infected during pregnancy. We investigated how the immune response to ZIKV during pregnancy is primed and conduct a thorough evaluation of the inflammatory and cytotoxic profiles as well as the expression of CCR5 and CX3CR1. We compared the reactivity of T cells to ZIKV peptides in convalescent mothers infected during pregnancy. The child's clinical outcome (i.e., born with or without CZS) was taken to be the variable. The cells were stimulated in vitro with ZIKV peptides and evaluated using the ELISPOT and flow cytometry assays. After in vitro stimulation with ZIKV peptides, we observed a tendency toward a higher Interferon gamma (IFN-γ)-producing T cell responses in mothers who had asymptomatic children and a higher CD107a expression in T cells in mothers who had children with CZS. We found a higher frequency of T cells expressing CD107a+ and co-expressing CX3CR1+CCR5+, which is much clearer in the T cells of mothers who had CZS children. We suggest that this differential profile influenced the clinical outcome of babies. These data need to be further investigated, including the evaluation of other ZIKV peptides and markers and functional assays.

Influence of chemokines on the endothelial permeability and cellular transmigration during dengue.

During a pathogenic infection, an inflammatory process is triggered in which several inflammatory mediators, such as cytokines, chemokines, growth factors, complement system components, nitric oxide, and others induce integrity alteration on the endothelial barrier. Chemokines are responsible for regulating leukocyte trafficking under homeostatic conditions as well as activating immune system cells under inflammatory conditions. They are crucial molecules in the early stages of infection, leading to the recruitment of immune cells, namely neutrophils, monocytes, natural killer (NK) cells, natural killer T cells (NKT), dendritic cells (DC), T lymphocytes and all cells expressing chemokine receptors for inflammatory sites. Other functions, such as collagen production, tissue repair, a proliferation of hematopoietic precursors and angiogenesis, are also performed by these molecules. Chemokines, amongst inflammatory mediators, play a key role in dengue immunopathogenesis. Dengue fever is a disease caused by the dengue virus (DENV). It is characterized by a broad spectrum of clinical manifestations ranging from asymptomatic cases to mild and severe symptomatic ones. As for the latter, the appearance of hemorrhagic manifestations and changes in vascular permeability may lead the patient to develop cavitary effusions, organ involvement, and even death. As chemokines exert an influence on various homeostatic and inflammatory processes, acting vigorously on vascular endothelial activation and cell migration, the main purpose of this chapter is to discuss the influence of chemokines on the alteration of endothelial permeability and migration of T lymphocytes in DENV infection.