Jila Masrour Roudsari

Mostafa Javanian

Soheil Ebrahimpour

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Immune Responses and Pathogenesis of Crimean–Congo Hemorrhagic Fever: An OverviewDear Editor,Crimean–Congo hemorrhagic fever (CCHF) is an emerging tick-borne (Ixodid ticks) viral infectious disease. CCHF is caused by RNA virus that is a member of genus Nairovirus in the family Bunyaviridae as the greatest virus family. This infection has vast geographical distribution in Asia, Africa and some parts of  Europe. This agent can be transmitted to humans in several ways such as direct contact with infected body fluids and blood or ticks. Small mammals are the main hosts of the virus. Although, domestic livestock present no clinical sign, they can transfer the disease during the period of viremia. The acute form of the infection usually lasts for two weeks and is characterized by prolonged weakness and confusion. Generally, the most common clinical signs and symptoms of this severe hemorrhagic viral disease include fever, headache, back pain, sore eyes, petechial rash, vomiting, and diarrhea. The mortality rate varies from 5% to 50% (1). Death is generally due to hemorrhagic and neurological complications (Figure 1). The pathogenesis of CCHF appears to be multifactorial, and it is poorly understood. However, an interaction between the virus and the host cells is known to be responsible for the pathogenesis of infection. The hepatocytes and endothelium are supposed to be the main target cells in CCHF. The infection of the hepatocytes leads to reduced synthesis of albumin as the main protein of human blood plasma, which can cause edema. Moreover, this hepatocyte dysfunction accounts for abnormal liver function tests (LFTs) (2). Endothelial damage can deregulate stimulation of platelet aggregation; on the other hand, it may contribute to coagulopathy. In addition, disseminated intravascular coagulation (DIC) is administrated by the activation of the clotting cascade that results in the formation of blood clots in the vessels. This pathological phenomenon can contribute to the activation of coagulation during CCHF (3). This virus can also infect antigen-presenting cells (APCs). The infected macrophages  or dendritic cells (DCs) release soluble factors such as cytokines. Several studies in CCHF reported that the release of tumor necrosis factor alpha Mostafa Javanian1, Jila Masrour Roudsari1, Soheil Ebrahimpour1*Open Access                                                                                                  Letter to EditorCrescent Journal of Medical and Biological Sciences Received 5 January 2017, Accepted 11 September 2017, Available online 19 October 2017 1Infectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, I.R. Iran.*Corresponding Author: Soheil Ebrahimpour, Tel: +989111149309, Email:drsoheil1503@yahoo.comhttp://www.cjmb.orgeISSN 2148-9696Vol. 5, No. 2, April 2018, 166–167                          Figure1. Pathogenesis of crimean congo hemorrhagic fever Figure 1. Pathogenesis of Crimean-Congo Hemorrhagic Fever.(TNF-α), Interleukin 6 (IL-6) and IL-10 may be engaged in the pathogenesis and outcome of the disease (4). TNF-α affects the endothelium and stimulates anti-fibrinolytic action. TNF-α and IL-6 are associated with DIC. Il-10 which can suppress the immune response to infection also allows high replication of the virus. Watson et al showed that the IL-12/IL-10 ratio is perhaps a useful procedure to approach the state of the immune system in CCHF (5,6). Some studies showed that there is a positive correlation between viral load and few proinflamatory cytokines and Javanian et al                                     Crescent Journal of Medical and Biological Sciences, Vol. 5, No. 2, April 2018 167also elevated levels of IFN-γ in cases with fatal outcomes of CCHF (7). Therefore, there are many vague points in the pathogenesis of CCHF that require further studies. In addition, a complete understanding of the pathogenesis may lead to more effective diagnostic and treatment designs. Conflict of Interests Authors declare that they have no conflict of interests. Ethical Issues Not applicable.Financial SupportNone.AcknowledgementsThe authors would like to thank department of infectious disease at Babol University of Medical Sciences,  Iran.References1. Soares-Weiser K, Thomas S, Thomson G, Garner P. Ribavirin for Crimean-Congo hemorrhagic fever: systematic review and meta-analysis. BMC Infect Dis. 2010;10:207. doi:10.1186/1471-2334-10-2072. Akinci E, Bodur H, Leblebicioglu H. Pathogenesis of Crimean-Congo hemorrhagic fever. Vector Borne Zoonotic Dis. 2013;13(7):429-437. doi:10.1089/vbz.2012.10613. Arslan M, Yilmaz G, Mentese A, Yilmaz H, Karahan SC, Koksal I. Importance of endothelial dysfunction biomarkers in patients with Crimean-Congo hemorrhagic fever. J Med Virol. 2017;89(12):2084-2091. doi:10.1002/jmv.248814. Papa A, Tsergouli K, Caglayik DY, et al. Cytokines as biomarkers of Crimean-Congo hemorrhagic fever. J Med Virol. 2016;88(1):21-27. doi:10.1002/jmv.243125. Papa A, Bino S, Velo E, Harxhi A, Kota M, Antoniadis A. Cytokine levels in Crimean-Congo hemorrhagic fever. J Clin Virol. 2006;36(4):272-276. doi:10.1016/j.jcv.2006.04.0076. Watson DC, Sargianou M, Panos G. Interleukin-12 (IL-12)/IL-10 ratio as a marker of disease severity in Crimean-Congo hemorrhagic fever. Clin Vaccine Immunol. 2012;19(5):823-824. doi:10.1128/cvi.00030-127. Saksida A, Duh D, Wraber B, Dedushaj I, Ahmeti S, Avsic-Zupanc T. Interacting roles of immune mechanisms and viral load in the pathogenesis of crimean-congo hemorrhagic fever. Clin Vaccine Immunol. 2010;17(7):1086-1093. doi:10.1128/cvi.00530-09Copyright © 2018 The Author(s); This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Immune Responses and Pathogenesis of Crimean–Congo Hemorrhagic Fever: An Overview

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