Intracellular Events and Cell Fate in Filovirus Infection
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 infec...
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doaj-e52af7b7f2954470b15ccb56e8e002b82020-11-24T21:13:50ZengMDPI AGViruses1999-49152011-08-01381501153110.3390/v3081501Intracellular Events and Cell Fate in Filovirus InfectionElena RyabchikovaRonald B. CorleyElke MühlbergerJudith OlejnikMarburg 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.http://www.mdpi.com/1999-4915/3/8/1501/Ebola VirusMarburg Virusfilovirusesviral replication cycletarget cellsanimal modelsultrastructural analysisvirus-cell interactionbystander apoptosiscell death |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Elena Ryabchikova Ronald B. Corley Elke Mühlberger Judith Olejnik |
spellingShingle |
Elena Ryabchikova Ronald B. Corley Elke Mühlberger Judith Olejnik Intracellular Events and Cell Fate in Filovirus Infection Viruses Ebola Virus Marburg Virus filoviruses viral replication cycle target cells animal models ultrastructural analysis virus-cell interaction bystander apoptosis cell death |
author_facet |
Elena Ryabchikova Ronald B. Corley Elke Mühlberger Judith Olejnik |
author_sort |
Elena Ryabchikova |
title |
Intracellular Events and Cell Fate in Filovirus Infection |
title_short |
Intracellular Events and Cell Fate in Filovirus Infection |
title_full |
Intracellular Events and Cell Fate in Filovirus Infection |
title_fullStr |
Intracellular Events and Cell Fate in Filovirus Infection |
title_full_unstemmed |
Intracellular Events and Cell Fate in Filovirus Infection |
title_sort |
intracellular events and cell fate in filovirus infection |
publisher |
MDPI AG |
series |
Viruses |
issn |
1999-4915 |
publishDate |
2011-08-01 |
description |
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. |
topic |
Ebola Virus Marburg Virus filoviruses viral replication cycle target cells animal models ultrastructural analysis virus-cell interaction bystander apoptosis cell death |
url |
http://www.mdpi.com/1999-4915/3/8/1501/ |
work_keys_str_mv |
AT elenaryabchikova intracellulareventsandcellfateinfilovirusinfection AT ronaldbcorley intracellulareventsandcellfateinfilovirusinfection AT elkemuhlberger intracellulareventsandcellfateinfilovirusinfection AT juditholejnik intracellulareventsandcellfateinfilovirusinfection |
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1716747965509402624 |