Summary

The syndrome of "viral hemorrhagic fever" in man caused bycertain viruses, such as Ebola, Lassa, Dengue, and Crimean-Congo hemorrhagic fever viruses, is often associated with ashock syndrome of undetermined pathogenesis. However, thevascular system, particularly the vascular endothelium, seems tobe directly and indirectly targeted by all these viruses. Here webriefly summarize the current knowledge on Marburg andEbola virus infections, the prototype viral hemorrhagic feveragents, and formulate a working hypothesis for the pathogenesisof viral hemorrhagic fever. Infections with filoviruses showlethality up to 89% and in severe cases lead to a shock syndromeassociated with hypotension, coagulation disorders and an imbalance of fluid distribution between the intravascular andextravascular tissue space. The primary target cells for filovirusesare mononuclear phagocytotic cells which are activatedupon infection and release certain cytokines and chemokines.These mediators indirectly target the endothelium and arethought to play a key role in the pathogenesis of filoviralhemorrhagic fever. In addition, direct infection and subsequentdestruction of endothelial cells might contribute to the pathogenesis.Filoviruses, particularly Ebola virus, encode nonstructuralglycoproteins which are released from infected host cells.Their function as potential determinants in pathogenicityremains to be investigated.