关键词: Ebola Virus Marburg Virus animal models bystander apoptosis cell death filoviruses target cells ultrastructural analysis viral replication cycle virus-cell interaction

Mesh : Animals Cell Death Cytopathogenic Effect, Viral Dendritic Cells / virology Filoviridae / chemistry pathogenicity physiology Filoviridae Infections / virology Genome, Viral Host-Pathogen Interactions Inclusion Bodies, Viral / ultrastructure Macrophages / virology Microscopy, Electron, Transmission RNA, Viral / genetics Viral Proteins / chemistry genetics Virus Cultivation Virus Internalization Virus Release Virus Replication

来  源:   DOI:10.3390/v3081501   PDF(Sci-hub)

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.
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