MARV had not been heard of for eight years, when a young Australian who had traveled throughout Zimbabwe was admitted to a hospital in Johannesburg, South Africa with symptoms reminiscent of those observed during the 1967 outbreak in Europe [8] . When he died and the infection spread to his travel companion and later also to a nurse, Lassa fever was initially suspected resulting in strict barrier nursing techniques and isolation of the patients and their primary contacts. This lead to a quick containment of the outbreak, and while the secondary cases recovered, MARV was identified as the causative agent of the disease. In the following years from 1975 through 1985, only sporadic outbreaks that affected small numbers of individuals were caused by MARV on the African continent (Table 1, Figure 1a ). As the case fatality rates associated with MVD were also lower than those seen in the devastating outbreaks associated with EBOV disease that reached up to 90%, MARV was long thought to be less threatening (Table 1) . However, this view had to be revised as MARV reemerged in two large outbreaks occurring in the Democratic Republic of the Congo (DRC) in 1998-2000 [9] and then, for the first time also in Western Africa, in Angola, in 2004-2005 [10] . The total number of 406 cases and the high fatality rates (83% in DRC and 90% in Angola) revealed that MARV was as big of a threat for public health as EBOV [1, 11] . The variation observed in disease severity and case fatality rates between these outbreaks versus the initial one in 1967 may depend on many complicating/mitigating factors. These include quality and availability of medical care, infectious dose and route of infection, differences in host population susceptibility (depending on immune and nutritional status) and genetics, inherent differences in viral variant virulence, and the prevalence of co-infections (particularly malaria and AIDS in patients from sub-Saharan Africa) [9] . The assumption that MARV Angola might be inherently more virulent than other MARV variants has been proposed mainly based on infection studies with nonhuman primates (NHP) [12] [13] [14] but is a matter of debate [15] . The genomes of the Angolan isolates differ about 7% at nucleotide level from the majority of the East African MARV isolates, including the ones from 1967 [10] . There is no evidence so far that the observed genetic differences result in higher virulence in humans.