Selective dysfunction of subsets of peripheral blood mononuclear cells during pediatric dengue and its relationship with clinical outcome

• Published in: Virology (New York, N.Y.) N.Y.), 2017-07, Vol.507, p.11-19
• Main Authors: Perdomo-Celis, Federico, Salgado, Doris M, Narváez, Carlos F
• Format: Article
• Language: English
• Subjects: Adolescent; Child; Child, Preschool; Cytokine; Dengue; Dengue - immunology; Dengue - virology; Dengue Virus - genetics; Dengue Virus - physiology; Female; Humans; Infant; Infectious Disease; Interferon; Interferon-alpha - immunology; Leukocytes, Mononuclear - immunology; Male; Monocytes; Monocytes - immunology; Pediatrics - statistics & numerical data; Plasmacytoid dendritic cell; T cells; Tumor Necrosis Factor-alpha - immunology
• ISSN: 0042-6822; 1096-0341
• DOI: 10.1016/j.virol.2017.04.004

Abstract During dengue virus (DENV) infection, a blockage of secretion of cytokines such as tumor necrosis factor (TNF)-α and members of the interferon (IFN) family has been described in vitro . We evaluated the functionality of monocytes as well as dendritic, B and T cells isolated from children with mild and severe dengue. Compared with those of healthy children, stimulated monocytes, CD4+ T cells and dendritic cells from children with dengue had lower production of proinflammatory cytokines. The interferon axis was dramatically modulated by infection as plasmacytoid dendritic cells (pDCs) and CD4+ T cells had low production of IFN-α and IFN-γ, respectively; plasma levels of IFN-α and IFN-γ were lower in severely ill children, suggesting a protective role. Patients with antigenemia had the highest levels of IFN-α in plasma but the lowest frequency of IFN-α-producing pDCs, suggesting that DENV infection stimulates a systemic type I IFN response but affects the pDCs function.