Ebola viruses (EBOV) are zoonotic pathogens that cause severe diseases in humans and have been responsible for several disease outbreaks over the past 40 years. Ebola virus disease (EVD) leads to death on an average of 45–50% of cases, but in some outbreaks, the figures have been higher. The largest EVD outbreak in West Africa in 2014–2015 lead to more than 28,000 cases and 11,300 fatalities. Host innate immune responses are vital in restricting the spread of viral infections including that of Ebola virus. EBOV and some other filoviruses are known to trigger uncontrolled virus replication by suppressing host innate immune responses, mainly by targeting the antiviral response through virus proteins. At least EBOV VP24 and VP35 proteins have been shown to inhibit the expression of type I and III interferon (IFN) genes as well as to inhibit IFN signaling leading to downregulated IFN-induced antiviral responses. In this review we concentrate on describing the mechanisms by which EBOV contributes to the pathogenesis of severe disease and on how the virus interacts with the host innate immune system.
Part of the book: Emerging Challenges in Filovirus Infections