Marburg and Ebola viruses, from the family Filoviridae, are prototype viral hemorrhagic fever pathogens that cause a fulminant hemorrhagic disease in humans and nonhuman primates. Following unspecific symptoms, patients display increased paraendothelial permeability, hypotension, coagulation disorders, hemorrhages and immune suppression.Disturbances of the blood tissue barrier, primarily controlled by endothelial cells, and immune suppression seem to be the key pathogenic factors of the disease. The endothelium is affected in two ways: Directly by virus infection leading to activation and perhaps lytic replication, and indirectly by a mediator-induced inflammatory response. Those mediators originate from virus-activated cells of the mononuclear phagocytic system which are the primary target cells. Immune suppression may result from lytic infection of circulating and sessile cells of the mononuclear phagocytic system, inactivation of neutrophils, impairment of antigen-presenting cells, and lymphoid depletion. Despite being clearly immunosuppressive, there is evidence of protective immunity during filovirus hemorrhagic fever. In contrast to survivors and asymptomatic cases that show humoral responses to viral antigens, fatal infections usually end with high viremia and little evidence of a humoral immune response. The transmembrane glycoprotein can be used to provoke a protective immune response in animal models including nonhuman primates.
|Title of host publication
|RNA Viruses: Host Gene Responses to Infections
|World Scientific Publishing Co.
|Number of pages
|9789812833808, 981283379X, 9789812833792
|Published - Jan 1 2009
ASJC Scopus subject areas
- General Immunology and Microbiology
- General Medicine