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Intracellular Events and Cell Fate in Filovirus Infection
Department of Microbiology, School of Medicine, Boston University, 72 East Concord Street, Boston, MA 02118, USA
National Emerging Infectious Diseases Laboratories Institute, Boston University, 72 East Concord Street, Boston, MA 02118, USA
Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of Russian Academy of Science, Pr. Lavrent’eva, 8, Novosibirsk 630090, Russian Federation
* Author to whom correspondence should be addressed.
Received: 7 June 2011; in revised form: 9 August 2011 / Accepted: 15 August 2011 / Published: 24 August 2011
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.
Keywords: Ebola Virus; Marburg Virus; filoviruses; viral replication cycle; target cells; animal models; ultrastructural analysis; virus-cell interaction; bystander apoptosis; cell death
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Olejnik, J.; Ryabchikova, E.; Corley, R.B.; Mühlberger, E. Intracellular Events and Cell Fate in Filovirus Infection. Viruses 2011, 3, 1501-1531.
Olejnik J, Ryabchikova E, Corley RB, Mühlberger E. Intracellular Events and Cell Fate in Filovirus Infection. Viruses. 2011; 3(8):1501-1531.
Olejnik, Judith; Ryabchikova, Elena; Corley, Ronald B.; Mühlberger, Elke. 2011. "Intracellular Events and Cell Fate in Filovirus Infection." Viruses 3, no. 8: 1501-1531.