Abstract
Dengue virus (DENV) is the most widespread arbovirus, responsible for a wide range of clinical manifestations, varying from self-limited illness to severe hemorrhagic fever. Dengue severity is associated with host intense proinflammatory response and monocytes have been considered one of the key cell types involved in the early steps of DENV infection and immunopathogenesis. To better understand cellular mechanisms involved in monocyte infection by DENV, we analyzed the expression levels of 754 human microRNAs in DENV-infected THP-1 cells, a human monocytic cell line. Eleven human microRNAs showed differential expression after DENV infection and gene ontology and enrichment analysis revealed biological processes potentially affected by these molecules. Five downregulated microRNAs were significantly linked to cellular response to stress, four to cell death/apoptosis, two to innate immune responses and one upregulated to vesicle mediated, TGF-β signaling, phosphatidylinositol mediated signaling, lipid metabolism process and blood coagulation.
Highlights
Dengue is an arthropod-borne viral disease that has rapidly spread around the world in the last decades and for which no antiviral treatment is currently available (Wilder-Smith et al, 2019)
No significant differences in cell viability were observed when mock-infected cells were compared to infected cells at this multiplicity of infection (MOI) (Figure S1C), ensuring that cell death related pathways would not bias further steps
Six independent experiments of activated THP-1 cells infected with dengue virus (DENV)-2 (MOI 10) for 24 hours were submitted to total RNA extraction followed by RT-qPCR expression analysis of 754 cellular microRNAs. microRNA profiles obtained were compared and, after clusterization, microRNA expression levels were sufficient to discriminate DENV-infected from mock-infected cells (Figure S2)
Summary
Dengue is an arthropod-borne viral disease that has rapidly spread around the world in the last decades and for which no antiviral treatment is currently available (Wilder-Smith et al, 2019). Dengue severity is linked to a host intense inflammatory response that leads to increased endothelial permeability and associated hemorrhagic manifestations. Different immune cell types are known to participate in the cytokine storm induced by dengue virus (DENV), including monocytes, macrophages, and dendritic cells (Cerny et al, 2014; Hottz et al, 2014; Alayli and Scholle, 2016; Bhatt et al, 2021). An increased number of activated monocytes have been found on blood samples from severe cases suggesting a key role for this cell type during DENV immunopathogenesis (Durbin et al, 2008). Monocytes play a central role in coordinating inflammation both by recruiting macrophages and dendritic cells and by inducing adaptive immunity (Jakubzick et al, 2017). Little is known about the mechanisms involved in monocyte responsiveness to DENV at the molecular level
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