Ebola virus, like the Marburg virus now alarming Angola, is a filovirus, a family of viruses that cause severe and frequently fatal hemorrhagic fevers. Zerhouni, M. Fauci, M. Senior author James M. Cunningham, M. Once this protein is snipped apart, the virus is free to begin multiplying. The scientists applied broad-spectrum enzyme inhibitors to mammalian cells before exposing them to Ebola virus.
When one specific cellular enzyme, cathepsin B, was inhibited, the infectivity of Ebola virus dropped to near zero. An accessory role is played by another cellular enzyme, cathepsin L, the scientists determined.
Although the vaccines would usually be months or even years away from approval, emergency protocols approved by the World Health Organization have determined that this epidemic warrants the use of unapproved drugs and vaccines, so cautious plans are being made to expand access to Ebola victims [7,8].
Another treatment which has been used for several health-care workers who became infected with Ebola virus involves the use of antibodies. Antibodies are large, Y-shaped proteins that are designed to recognize and neutralize foreign objects in your body, such as bacteria or viruses. Currently, the most well developed drug is called ZMapp, which is a cocktail of three antibodies. Once bound, the antibodies neutralize the glycoprotein, which subsequently keeps the virus out of the cell.
So far, data about its efficacy in humans has been inconclusive, as the patients did not all receive the drug at the same point in the course of their disease, nor did they receive the same levels of medical care [10]. ZMapp or other similar drugs are important as tools to treat already infected patients during an outbreak, but unlike a vaccine, they do not confer lifelong immunity to the virus. This ultimately means that exploring both vaccines and drug treatments may be the most effective way to combat Ebola.
Even if experimental drugs can be scaled up to have large enough quantities to treat the current epidemic, the traditional methods of treatment will continue to be paramount for saving lives. In order to stave off shock from loss of blood and fluids, patients in health-care facilities can be given infusions of blood, fluids and electrolytes to help their bodies remain stable while fighting the virus.
In the immediate future, the major challenges in bringing this epidemic under control will continue to be a focus on its containment, coupled with an influx of health-care facilities and experts capable of delivering the best care possible in onerous conditions. September Ebola are virus so they need a cell to produce offspring. They are like robots. EBOV entry into the cells is initiated by the interaction of the viral GP with receptors on the surface of host cells, and then internalized via macropinocytosis pathway.
Several host enzymes which remain to be fully characterized are regarded to catalyse the reaction. This is a challenge for researchers as there are abundant enzymes involved within host cells. During assembly and budding, GP2 antagonizes the anchoring of tetherin via unarticulated mechanisms; VP40 regulates viral budding by associating with the inner leaflet of the plasma membrane with unknown detailed mechanisms. Therefore, the aspects that remain unclear in the EBOV lifecycle is waiting for profound research.
National Center for Biotechnology Information , U. Journal List Oncotarget v. Published online Jun Frederick X. Author information Article notes Copyright and License information Disclaimer. Correspondence to: Hang-Ping Yao, nc.
Lan-Juan Li, nc. Received Apr 21; Accepted May This is an open-access article distributed under the terms of the Creative Commons Attribution License 3. This article has been cited by other articles in PMC. Abstract Ebola haemorrhagic fever causes deadly disease in humans and non-human primates resulting from infection with the Ebola virus EBOV genus of the family Filoviridae.
Open in a separate window. Figure 1. Uptake Filoviruses virions are uptaked into host cells involve different endocytic pathways. Uncoating and fusion Following endocytosis, the next steps consist of the uncoating and fusion of the viral membrane with the endosomal membranes.
Assembly and budding Assembly of viral particles begins with the formation of nucleocapsids which accumulate in the perinuclear region and are transported to the budding sites at the plasma membrane. Figure 2. Unincorporated entry methods, unidentified proteins or receptors, un-illuminated pathways in different cell lines. Uncoating and Fusion GP-mediated, host enzyme cooperation Unidentified enzymes trigger and accelerate the process.
Transcription and Replication RNP i. The molecular mechanism of RNP is unclear. How does NP complete its function? How does VP24 contribute to assembly and budding? What is the mechanism used to control VP40 oligomerization? How does myosin influence the localisation of intra-filopodia motility release? How does VP40 associate with the inner leaflet? Ebolavirus comparative genomics. Neglected filoviruses. Slenczka WG. The Marburg virus outbreak of and subsequent episodes.
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J Vet Med Sci. Cell Reports. Insight into the Ebola virus nucleocapsid assembly mechanism: crystal structure of Ebola virus nucleoprotein core domain at 1. Protein Cell. The Ebola virus VP35 protein inhibits activation of interferon regulatory factor 3.
J Virol. A C-terminal basic amino acid motif of Zaire ebolavirus VP35 is essential for type I interferon antagonism and displays high identity with the RNA-binding domain of another interferon antagonist, the NS1 protein of influenza A virus. Stahelin RV. Membrane binding and bending in Ebola VP40 assembly and egress. Front Microbiol. Oligomerization of Ebola virus VP40 is essential for particle morphogenesis and regulation of viral transcription.
Processing of the Ebola virus glycoprotein by the proprotein convertase furin. Release of viral glycoproteins during Ebola virus infection. Nat Med. Antigenic subversion: a novel mechanism of host immune evasion by Ebola virus. PLoS Pathog. A virus factor of cell entry is a surface glycoprotein GP , which is an only essential viral protein in the step, as well as the unique particle structure.
The virus also interacts with a lot of host factors to successfully enter host cells.
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