Replication of Ebola Virus can be Terminated by Mutating its Key Protein
Researchers were able to terminate the replication of Ebola virus by mutating Viral Protein (VP40), according to a study conducted on March 12, 2018.
Viral budding from the plasma membrane is regulated by VP40, which is a peripheral membrane protein. Replication of the virus is facilitated by the interaction of this protein with a human plasma-membrane lipid known as phosphatidylserine. For entry and exit through the cells, viruses have to cross the membranes. Specific parts of this protein that bind with the lipid was found by the researchers. The ability of the protein to form a protective layer is controlled by this lipid. If membrane penetration and budding has to take place, presence of water-attracting residues at the site are critical. When these residues were replaced with alanine, lipid binding was reduced by 40-fold.
Currently, there are no vaccines or treatments available to cure Ebola virus. Targeted therapeutics can be developed once the researchers are able to understand how and where the interaction between protein and lipids take place. Robert Stahelin, a researcher said, “This helps us understand how the virus uses human cell membranes to replicate and form new virus particles. The virus needs this one lipid to form the new particle and infect other cells.” This study used cellular and vitro models.
To quantify how well VP40 can bind to synthetic membranes, vitro models were used. The amino acid sequence of the protein was altered by mutating the DNA code. Then, those proteins were purified to homogeneity and their bindings were compared to that of the original VP40. To monitor VP40 localization in human cells, live cell imaging was used in cellular experiments. This study will be beneficial for an increase in the growth of Ebola vaccine market, as elaborated in the Ebola vaccine market report published by Coherent Market Insights.
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