The role of Treg population in pathogenesis of Crimean Congo hemorrhagic fever

• Published in: Virus research Vol. 250; pp. 1 - 6
• Main Authors: Gazi, Umut, Yapar, Derya, Karasartova, Djursun, Gureser, Ayse Semra, Akdogan, Ozlem, Unal, Ozgur, Baykam, Nurcan, Taylan Ozkan, Aysegul
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 02.05.2018
• Subjects: Crimean-Congo hemorrhagic fever (CCHF); Immunity; Pathogenesis; Regulatory T-cells (Treg); Crimean-Congo hemorrhagic fever (CCHF); Pathogenesis; Immunity; Regulatory T-cells (Treg)
• ISSN: 0168-1702; 1872-7492
• DOI: 10.1016/j.virusres.2018.04.003

•Acute CCHFV infection does not cause any change in T-cell and helper T-cell levels.•Acute CCHF patients displayed higher Treg cell levels.•Lower Treg suppressive activies were reported in acute CCHF patients. Crimean-Congo hemorrhagic fever (CCHF) is a severe human infection caused by CCHF virus (CCHFV). Today, although the literature on CCHF pathogenesis is still limited, it is thought to be associated with immunosuppression in the early phase of infection followed by pro-inflammatory immune response that may lead to fatal outcomes. The aim of this study is to investigate the role of regulatory T-cells (Treg cells) in the pathogenesis of CCHFV. Peripheral blood mononuclear cell samples collected from 14 acute CCHF patients with mild disease course and 13 healthy subjects were included in this study. Treg expression and functional levels were analyzed by flow cytometry. Treg cells were identified as CD4+CD25 + CD127dim cells, and their functional levels were compared by measuring their ability to suppress CD69 and CD154 expression by activated T-cells. The flow cytometry analysis revealed that total T-cell and helper T-cell levels did not vary between the two groups. In contrast, CCHF patients displayed higher Treg cell levels but lower Treg suppressive activities when compared with control subjects. This is the first study on the involvement of Treg cells in CCHF pathogenesis. Our results indicate that even though Treg cell levels are elevated during acute phase of CCHF infection, not all generated Treg cells has immunosuppressive capacity, and therefore may not represent ‘true’ Treg cell population. Future studies on the intrinsic mechanisms responsible for the reduced Treg inhibitory activities are required for further enlightening the CCHF pathogenesis, especially in the acute phase of the disease.