Summary
The syndrome of “viral hemorrhagic fever” in man caused by certain viruses, such as
Ebola, Lassa, Dengue, and Crimean-Congo hemorrhagic fever viruses, is often associated
with a shock syndrome of undetermined pathogenesis. However, the vascular system,
particularly the vascular endothelium, seems to be directly and indirectly targeted
by all these viruses. Here we briefly summarize the current knowledge on Marburg and
Ebola virus infections, the prototype viral hemorrhagic fever agents, and formulate
a working hypothesis for the pathogenesis of viral hemorrhagic fever. Infections with
filoviruses show lethality up to 89% and in severe cases lead to a shock syndrome
associated with hypotension, coagulation disorders and an imbalance of fluid distribution
between the intravascular and extravascular tissue space. The primary target cells
for filovi-ruses are mononuclear phagocytotic cells which are activated upon infection
and release certain cytokines and chemokines. These mediators indirectly target the
endothelium and are thought to play a key role in the pathogenesis of filoviral hemorrhagic
fever. In addition, direct infection and subsequent destruction of endothelial cells
might contribute to the pathogenesis. Filoviruses, particularly Ebola virus, encode
nonstructural glycoproteins which are released from infected host cells. Their function
as potential determinants in pathogenicity remains to be investigated.
Keywords
Filoviruses - influenza virus - endothelium - cytokines
