Conference abstract

Lower activation-induced T-cell apoptosis is related to the pathological immune response in secondary infection with hetero-serotype Dengue virus

Pan African Medical Journal - Conference Proceedings. 2017:4(44).21 Dec 2017.
doi: 10.11604/pamj-cp.2017.4.44.416

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Keywords: Dengue, serotype DENV, immune response, apoptosis
Abstract

Lower activation-induced T-cell apoptosis is related to the pathological immune response in secondary infection with hetero-serotype Dengue virus

Jintao Li1,&, Huacheng Yan1, Tiantian Yu1, Hongxia Guo1, Nan Ye1, Yue Chen1, Ruiwen Ren1

1Institute of Tropical Medicine, Third Military Medical University, China

&Corresponding author
Jintao Li, Institute of Tropical Medicine, Third Military Medical University, China

Abstract

Introduction: the available evidence suggests that dengue virus-specific T-lymphocytes and cytokine storm play a pivotal role in the immune-pathogenesis of plasma leakage. Investigations are underway to identify the immune profiles associated with increased or decreased risk for severe disease.

Methods: in this study, CD14+ cells from the peripheral blood mononuclear cells (PBMCs) of patients who recovered from DENV-1 infection were infected with DENV-1 or DENV-2 and co-cultured with memory T-cells.

Results: we found that secondary infection with DENV-2 suppresses the cell reproductive capacity but forms more cell clones and more functional cells to produce more pro-inflammatory factors (IFN-γ, TNF-α, IL-6, IL-8, IL-12 and IL-17) and less regulatory cytokines (IL-10, TGF-β) which results in higher viral replication compared to secondary infection with DENV-1. Memory dengue virus-specific T-cells which are induced in a primary dengue virus infection are reactivated by the heterologous serotype of dengue virus and antigen presenting cells (APCs) during a secondary infection. Dramatically, less apoptosis and more continuous activation of T-cells in secondary infection with hetero-serotype DENV were observed. This discovery which has not been reported previously may be the reasonable and vital interpretation for the cytokine storm and severe symptoms observed in secondary infection with DENV.

Conclusion: secondary infection with hetero-serotype DENV elicits the relatively pathological immune response while secondary infection with homologous-serotype DENV induces the relatively protective immune response by activation-induced cell death (AICD) of T-cells.