INTRODUCTION

Filoviruses cause fulminant haemorrhagic fever in humans and non-human primates, killing up to 90 % of the infected patients. Since the discovery of Marburg virus (MBGV) in 1967 and the emergence of Ebola virus (EBOV), its better known cousin, a few years later, these infections have therefore been a matter of high public and scientific concern. Although it is clear from the recorded history of filovirus outbreaks that all of them have so far been self-limiting and that the total number of human infections hitherto documented scarcely exceeds a thousand cases, EBOV by now ranges among the most ill-famed human viruses. For a long time, research on filoviruses has been impeded by their high pathogenicity, but with the advent of recombinant DNA technology our knowledge of the genome structures and the replication strategies of these agents has increased significantly.

PATHOPHYSIOLOGY OF FILOVIRUS INFECTIONS

The pathophysiological changes that make filovirus infections so devastating are just beginning to be unravelled. Pathogenesis in fatal infections in human and non-human primates is similar, suggesting the primate system is a reasonable model for studying filovirus haemorrhagic fever (Simpson et al., 1968; Murphy et al., 1971; Ellis et al., 1978; Fisher- Hoch et al., 1985; Ryabchikova et al., 1994). Clinical and biochemical findings support the anatomical observations of extensive liver involvement, renal damage, changes in vascular permeability, including endothelial damage, and activation of the clotting cascade. The visceral organ necrosis is a consequence of virus replication in parenchymal cells. However, no organ, not even the liver, shows sufficient damage to account for death.

Fluid distribution problems and platelet abnormalities are dominant clinical manifestations, reflecting damage of endothelial cells and decrease of platelets.