|Letters to Editor|
|Immune Responses and Pathogenesis of Crimean–Congo Hemorrhagic Fever: An overview|
|Mostafa Javanian1, Jila Masrour Roudsari1, Soheil Ebrahimpour1|
|1Infectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran|
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Keywords : crimean–congo hemorrhagic fever, Pathogenesis, Cytokine
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Crimean–Congo hemorrhagic fever (CCHF) is as an emerging tick-borne (Ixodid ticks) viral infection disease. CCHF 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; as direct contact with infected body fluids and blood or ticks. Small mammals are serious bolster hosts of the virus. Although, domestic livestock present no clinical sign present but can transfer the disease during period of viremia. The acute form of the infection usually lasts withintwo weeks and characterized by prolonged weakness and confusion. Generally, the most common clinical signs and symptoms of this severe hemorrhagic viral diseaseincluding fever,headache, back pain,sore eyes, petechial rash, vomiting, and diarrhea.The mortality ratehas varied from 5-50%(1). Death is generally due to hemorrhagic and neurologicalcomplications (Figure1).The pathogenesis of CCHF appears to be multifactorial, and itis poorly understood. But as it is known, an interaction between the virus and the host cells is responsible for the pathogenesis of infection. Thehepatocytesand endothelium aresupposed to be the main target cells in CCHF. The infection of the hepatocytes leadsreduced synthesis in albumin as the main protein of human blood plasma, which can cause to edema. Moreover, this hepatocyte dysfunction reasons to abnormal liver function tests (LFT) (2). Endothelial damage can deregulate stimulation of platelet aggregation, in the other hand, it may contribute to coagulopathy. Also, disseminated intravascular coagulation (DIC) is administrated by activation of the clotting cascade that results in the formation of blood clots in the vessels. This pathological phenomenon can contribute toactivation of coagulation during CCHF (3). This virus also can infect antigen presenting cells (APCs). The infected macrophages or dendritic cells (DCs) release soluble factors as cytokines. Several studies in CCHF reported that the release of TNF-α, IL-6 and Il-10 which may be engaged in the pathogenesis and outcome of the disease(4).TNF-α effects on the endothelium and stimulates anti-fibrinolytic action. TNF-α and IL-6 are associated with DIC. Il-10 which can suppress immune response to infection also allows high replication of the virus, so that Watson et al, showed that the IL-12/IL-10 ratio is perhaps useful procedure to approach the state of the immune system in CCHF (5, 6).Some researches showed that the positive correlation was between viral load and few pro inflammatory cytokines and also, 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, complete understanding of the pathogenesis may lead to more effective diagnostic and treatment designs.
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