Ebola’s exploits: debilitating host immune responses through interferon inhibiting domains
The recent Ebola virus disease (EVD) outbreak in West Africa was unprecedented in human suffering (over 28,000 reported cases, more than 11,000 deaths), timespan [2014–2016], and geographic scope (epidemic spread in Guinea, Liberia, and Sierra Leone with exportation of cases to multiple continents) (1). Ebola virus (EBOV), an etiologic agent of acute hemorrhagic fever, usually results in high case fatality rates. At least part of the virulence of EBOV is attributed to its tropism for cells of the innate immune system: monocytes, macrophages, and immature dendritic cells (2,3). Upon infection, EBOV actively dampens intrinsic antiviral immune defenses, causing systemic immunosuppression, lymphocyte apoptosis, and lymphopenia. In fatal cases, these hallmarks of EVD and the accompanying innate immune disarmament allow unfettered viral replication within the host, resulting in a highly lethal disease with extreme pathogenic characteristics. The 2014 EBOV outbreak renewed interest in characterizing EBOV immunoevasion strategies, primarily occurring through viral antagonism of type I interferons (IFN-I), which may be critical components of vaccine and antiviral therapeutic applications for controlling future EBOV outbreaks.