Content area
Full Text
Filoviruses are negative strand RNA viruses within the order of Mononegavirales [1]. Both members of the Filoviridae family, Ebola virus [EBOV; species Zaire ebolavirus (ZEBOV), Sudan ebolavirus (SEBOV), Taï Forest ebolavirus and Bundibugyo ebolavirus (BEBOV)] and Marburg virus (MARV; species Lake Victoria marburgvirus ), cause a severe form of viral hemorrhagic fever in humans with case fatality rates up to 90% [1]. MARV originates from Africa but was discovered in 1967 during an outbreak in Marburg, Germany. EBOV was identified 9 years later in 1976 in Central Africa with two simultaneous outbreaks in Sudan and Zaire (now Democratic Republic of the Congo) (Figure 1). In the past two decades, EBOV hemorrhagic fever (EHF) epidemics were frequently reported from Central Africa and continue to emerge/re-emerge; for example, in 2012 dozens of EBOV cases were identified in Uganda and in the Democratic Republic of the Congo (Figure 1) [2,3]. Noteworthy, since the beginning of the millennium, EHF outbreak locations have moved from the border region of Gabon and the Republic of Congo (ZEBOV outbreaks) to the east (BEBOV and SEBOV outbreaks) accompanied by a change in the EBOV species causing the infections (Figure 1). Although EBOV pathogenesis has been well characterized in animal disease models, particularly the macaque models, and the limited data available from human cases, there is still no licensed vaccine or treatment available. EBOV is a category A pathogen and can only be handled in maximum containment laboratories.
Figure 1. Ebola hemorrhagic fever outbreaks in Africa since discovery in 1976. Maps depicting documented outbreaks of Ebola hemorrhagic fever in Africa for the last five decades. 1970s - five documented outbreaks; 1980s - no reported outbreaks; 1990s - six confirmed outbreaks; 2000s - 10 documented outbreaks; 2010s - so far five confirmed outbreaks.
(Figure omitted. See article PDF.)
The 'gold standard' animal disease models for EBOV are the rhesus and cynomolgus macaque, which can be infected with nonadapted virus strains. Immunocompetent rodent models are not commonly available for EBOV species with the exception of ZEBOV. For ZEBOV mouse, hamster and guinea pig disease models have been established using either mouse-adapted (MA-ZEBOV) or guinea pig-adapted (GPA-ZEBOV) challenge strains [4,5]. While the rodent disease models show limitations in representing certain aspects of EHF in humans, the...