Abstract
Crimean-Congo hemorrhagic fever virus (CCHFV) is a widely distributed hemorrhagic fever virus and the cause of hemorrhagic disease in Africa, Southern and Eastern Europe, the Middle East, India and Asia. Recent emergence of CCHFV into Spain indicates that the geographic range of this virus is expanding and the presence of its tick vector in several countries without reported disease suggest that CCHFV will continue to spread. Research into CCHFV was historically limited by a lack of suitable animal models and tools to study viral pathogenesis. However, in the past few years the toolset for studying CCHFV has expanded with small animal and non-human primate models for CCHFV being developed along with a reverse genetics system that allows for investigation of viral determinants of disease. These tools have been utilized to understand how CCHFV antagonizes host restriction factors and to develop novel vaccine candidates that may help limit the substantial morbidity and mortality in humans caused by CCHFV.
Highlights
Crimean–Congo hemorrhagic fever virus (CCHFV) is a negativesense RNA virus in the Nairoviridae family within the Bunyavirales order of viruses
The main vector and reservoir of Crimean-Congo hemorrhagic fever virus (CCHFV) are hard-body ticks principally of the Hyalomma genus, there is limited evidence that other species of ticks such as Rhipicephalus and Dermacentor species may be vectors[3]. Vertebrate hosts such as domestic livestock and wild animals such as hares likely serve as amplifying hosts of CCHFV, with uninfected ticks becoming infected during feeding on viremic animals or during co-feeding with infected ticks[4,5,6] (Figure 1)
Summary In conclusion, much remains to be understood about the pathogenesis of CCHFV
Summary
Crimean–Congo hemorrhagic fever virus (CCHFV) is a negativesense RNA virus in the Nairoviridae family within the Bunyavirales order of viruses. Data in humans and mice suggest that while ribavirin may have limited clinical benefit in patients with CCHF, treatment likely needs to be started early in the course of disease to have clinical benefit This may prove difficult, as the early symptoms of CCHF are non-specific and can progress rapidly to severe, hemorrhagic manifestations[8] and patients may not present to healthcare providers until exhibiting the more serious symptoms of CCHF. The toolset for studying CCHFV has been steadily improving in recent years with the development of mouse and non-human primate models to a reverse genetics system for CCHFV that will facilitate dissection of the host and viral determinants of CCHFV pathogenesis These tools will allow the development and evaluation of novel therapies that reduce or prevent CCHFV-induced morbidity and mortality. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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