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Scientists have managed to inhibit the reproduction of ebola virus in laboratory conditions. Whether the breakthrough can translate into an actual drug is an open question, but the good news is that if it can, the product is likely to work on all ebola strains and maybe on some other vicious viruses as well.
The team isnt suggesting a cure, its suggesting a way to stop the virus, which causes a deadly hemorrhagic disease, from multiplying.
Like all viruses, ebola is incurable; no treatment exists. Doctors can only try to boost the patients immune system and hope this does the job. Also, like all viruses, ebola is a complete parasite. Other parasites may need the host to survive, but without a host, a viral particle might as well be a rock. Viruses are the only known form of life that cannot proliferate on their own. They depend on their hosts.
Instead of dividing into two, like bacteria or amoebae, viruses hijack host cells. They inject their genetic material into the cell and it take over. Instead of making whatever it needs to make, the cell becomes a virus factory creating new virus particles.
The current breakthrough is that scientists in Copenhagen have identified a human enzyme crucial to this hijacking quality by ebola. They have demonstrated that inhibiting an enzyme called PP2A-B56 stops ebola from proliferating, as reported in Molecular Cell.
PP2A-B56 is an enzyme that is present in all human cells and is hijacked by the virus to promote its own transcription, explains Prof. Jakob Nilsson of the Novo Nordisk Foundation Center for Protein Research at the University of Copenhagen. Without it, the virus is not able to produce new copies of itself, he told Haaretz.
Under normal (uninfected) conditions, PP2A-B56 is involved in regulating a number of our metabolic processes. In other words, we need this enzyme for our cells and bodies to function normally. But when we're infected, specifically inhibiting PP2A-B56 stops the cell from making more ebolas.
This material was created specially for WorldHealthNews project by John Bates.
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