Nevertheless, the lack of type I interferon in these models limits their usefulness for studying innate immunity to CCHFV, the rapid onset lethal disease in most of these models precludes study of later host responses and lack of type I interferon can impact adaptive immunity following infection or vaccination ( Clarke and Bradfute, 2020). Infection of these mice typically results in a rapid onset fatal disease with many similarities to fatal human cases ( Zivcec et al., 2013 Bente et al., 2010), although our group has recently developed a model that recapitulates the convalescent phase of CCHF ( Hawman et al., 2019). To date, mouse models of CCHF have been limited to mice deficient in type I IFN responses, either through genetic deficiency such as interferon alpha receptor knock-out ( Ifnar1 -/-) ( Zivcec et al., 2013 Bente et al., 2010 Bereczky et al., 2010) or through transient deficiency by antibody-mediated blockade of the interferon alpha receptor ( Garrison et al., 2017 Lindquist et al., 2018).
Case fatality rates can be as high as 30% ( Bente et al., 2013). CCHF begins as a non-specific febrile illness that can rapidly progress to hemorrhagic disease ( Ergönül, 2006), and there are currently no widely approved vaccines nor antivirals for CCHF. Climate change is leading to expansion of the range for Hyalomma ticks and recently Hyalomma ticks were found as far north as Sweden ( Grandi et al., 2020). Ticks of the Hyalomma genus are the principal vector and reservoir for CCHFV and cases of CCHF closely follow the geographic range of Hyalomma ticks ( Bente et al., 2013).
CCHFV is among the most widely distributed hemorrhagic fever viruses with cases reported through Africa, the Middle East, Asia, and Southern and Eastern Europe ( Bente et al., 2013). Crimean-Congo hemorrhagic fever virus (CCHFV) is the cause of Crimean-Congo hemorrhagic fever (CCHF).
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