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Molecular genetics and microbiology of Zaire Ebolavirus


Ebola virus disease (EVD) is a life-threatening condition caused by Zaire Ebolavirus (EBOV) which has been associated with mortality rates as high as 90, percent. The disease pathology observed in EVD remains unclear, though it appears that death is due to a paradoxical combination of aberrant coagulation and severe hemorrhage from small blood vessels.
EBOV is a negative-sense, single-stranded RNA virus, composed of a helical RNA strand wrapped about several structural and regulatory proteins including VP35, VP30, nucleoprotein (NP) and Protein L within the capsid. VP35 and VP30 act as cofactors to Protein L, which catalyzes transcription of the viral RNA within the cytosol of the host cell. The capsid is surrounded by an envelope derived from the host cell’s plasma membrane, which is studded with 10nm spikes of viral glycoprotein (GP). The structure of EBOV is shown in Figure 1.
Figure 1: Structure of Ebolavirus.
Unlike positive-sense (5, ’ to 3, ’) RNA viruses—such as poliovirus— the pure, isolated RNA from EBOV is not inherently infectious. The viral genome of negative-sense (3, ’ to 5, ’) pathogens must first be transcribed to produce functional viral mRNA. In comparison, the viral genome of poliovirus and other positive-sense pathogens, can be immediately translated by the host cell into necessary viral proteins.
The mechanism by which EBOV enters the host cell is still a topic of debate. A hypothetical research study hopes to examine if entry is achieved via clathrin-mediated endocytosis, the details of which are shown in Figure 2. Poliovirus is known to infect cells by this mechanism. After binding to a receptor in a clathrin-coated pit, the virus is enveloped in a vesicle. The vesicle is pinched off by the action of the key protein dynamin, which progressively tightens around the budding vesicle like a belt, until it is entirely endocytosed.
Figure 2: Clathrin-mediated endocytosis.
(I) Ligands bind to receptors on the cell surface, forming a clathrin coated pit. (II) More clathrin is recruited to coat the budding vesicle; dynamin beings to polymerize. (III) Dynamin constricts around the budding vesicle. (IV) The vesicle is pinched off from the plasma membrane, and enters the cell.
In this fictional study, the experimenters create two experimental groups. In group 1, 100 rats are infected with live poliovirus, and in group 2, 100 rats are infected with live EBOV. For each group, half of the rats (50) are then injected with “drug X”, a drug known to inhibit dynamin. After two weeks in this hypothetical experiment, the animals are euthanized, biopsies are taken, and immunohistochemical staining is used to identify the number of infected cells per high-powered microscope field. Figure 3 shows the idealized result of this hypothetical scenario.
Figure 3: Effect of drug X on viral infectivity.
The average percentage of infected cells per high power field are shown pre and post treatment with Drug X for the rats inoculated with poliovirus and EBOV. The black bars represent standard error.
From the results in Figure 3, what can be concluded about EBOV’s mechanism of cell entry, and why?
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