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Abstract
Marburg and Ebola viruses cause a severe hemorrhagic disease in humans with high fatality rates. Early target cells of filoviruses are monocytes, macrophages, and dendritic cells. The infection spreads to the liver, spleen and later other organs by blood and lymph flow. A hallmark of filovirus infection is the depletion of non-infected lymphocytes; however, the molecular mechanisms leading to the observed bystander lymphocyte apoptosis are poorly understood. Also, there is limited knowledge about the fate of infected cells in filovirus disease. In this review we will explore what is known about the intracellular events leading to virus amplification and cell damage in filovirus infection. Furthermore, we will discuss how cellular dysfunction and cell death may correlate with disease pathogenesis.
Highlights
The members of the filovirus family, Ebola virus (EBOV) and Marburg virus (MARV), cause a severe hemorrhagic fever in infected humans with high fatality rates [1]
Infected individuals who go on to succumb to filovirus infection exhibit dysregulated immune responses
T-cell immunoglobulin and mucin domain 1 (TIM-1) is not expressed by the primary targets of filoviruses, macrophages and dendritic cells (DCs), but is expressed on mucosal epithelial cells, whose role in infection is not clear yet
Summary
The members of the filovirus family, Ebola virus (EBOV) and Marburg virus (MARV), cause a severe hemorrhagic fever in infected humans with high fatality rates [1]. The first reported MARV outbreak occurred in Germany and Yugoslavia in 1967 and was caused by infected African green monkeys imported from Uganda [18,19] Since this outbreak was associated with a case fatality rate of 22%, it was believed for a long time that MARV was less pathogenic than. Despite the severity of the disease, filoviruses have been regarded as exotic pathogens with fatal outbreaks restricted to Central Africa, and with no major health threat outside of the endemic areas. Knowledge on their biology and pathogenicity remained limited. Present ultrastructural data of infected and non-infected cells, demonstrating the morphological changes in filovirus infection
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