Abstract
The worst Ebola virus (EV) outbreak in history has hit Liberia, Sierra Leone and Guinea hardest and the trend lines in this crisis are grave, and now represents a global public health threat concern. Limited therapeutic and/or prophylactic options are available for people suffering from Ebola virus disease (EVD) and further complicate the situation. Previous studies suggested that the EV glycoprotein (GP) is the main determinant causing structural damage of endothelial cells that triggers the hemorrhagic diathesis, but molecular mechanisms underlying this phenomenon remains elusive. Using the informational spectrum method (ISM), a virtual spectroscopy method for analysis of the protein-protein interactions, the interaction of GP with endothelial extracellular matrix (ECM) was investigated. Presented results of this in silico study suggest that Elastin Microfibril Interface Located Proteins (EMILINs) are involved in interaction between GP and ECM. This finding could contribute to a better understanding of EV/endothelium interaction and its role in pathogenesis, prevention and therapy of EVD.
Highlights
Ebola virus (EBOV) is an aggressive pathogen that causes a highly lethal hemorrhagic fever syndrome in humans and nonhuman primates with mortality rates ranging from 50 to 90% (Peters and Khan, 1999)
To identify the common information encoded by EBOV GP1 and C1q, informational spectrum method (ISM) analysis was performed on all non-redundant EBOV-2014 GP1 amino acid sequences in GenBank (Data Sheet 2)
The Ebola virus (EV) disease (EVD) is a multisystemic disease which is characterized by hypotension, generalized fluid distribution balance, lymphopenia, coagulopathy, and hemorrhage
Summary
Ebola virus (EBOV) is an aggressive pathogen that causes a highly lethal hemorrhagic fever syndrome in humans and nonhuman primates with mortality rates ranging from 50 to 90% (Peters and Khan, 1999). EBOV belongs to the Filoviridae, order Mononehavirales The members of this genus of ssRNA viruses are called ebolaviruses and include five known virus species: Bundibugyo virus (BDBV), Sudan virus (SUDV), Taï Forest virus (TAFV), Reston virus (REBOV) and one called Ebola virus (EBOV, formerly Zaire Ebola virus) which caused a number of outbreaks during the past 40 years. S408G, which was absent from all the EBOV isolates after 1996, into EBOV KM233035 GP1 resulted in a significant increase of the amplitude at the frequency F(0.338) (Figure 6) This suggests that acquisition of this mutation by EBOV during the current outbreak in West Africa could increase its interaction with ECMs expressing EMILINs, as already proposed by our work for the PA from B. anthracis and EMILINs (Doliana et al, 2008). These results support our assumption about significance of these mutations which could help the virus to avoid the host immune response
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