Researchers Use Mutated Gene To "Handicap" Ebola Virus Growth

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Robin Andrews 04 Nov 2015, 22:40

The recent outbreak of Ebola, concentrated on three countries in West Africa, has claimed over 11,000 lives. Research on potential vaccines to this virus has been ongoing, and a medical team at the University of Pennsylvania may have developed a novel way to combat the deadly infection: By temporarily handicapping the virus, the body’s immune system is given time to develop a more robust response. The findings are reported in the journal PLOS Pathogens.

Ebola is a type of hemorrhagic virus, a pathogen that causes the host to experience potentially life-threatening excessive bleeding, along with a powerful fever. The virus is fast-acting, with the course of infection – from exposure to death – taking as little as two weeks to occur. The immune system, more often than not, fails to build up an effective response to the virus in such a short time.

This new research, pioneered by Bruce Freedman and Ronald Harty in the Department of Pathobiology at the University of Pennsylvania School of Veterinary Medicine, is a type of antiviral therapy, in this case one specifically designed to buy the immune system more time when the body is under viral attack.

Viruses replicate themselves by hijacking the host cell’s machinery, in effect “hacking” the programming of the cell and causing it to produce copies of the virus’ genetic material. The researchers thought that messing around with the host cell’s processes would ultimately disrupt the proliferation of the Ebola virus.

Within cells, signals – involving electrically excited particles called ions – are used by the cell to respond to changes in their microenvironment, and to govern their internal processes. Calcium ions are a commonly used signaling ion, and the researchers found that the Ebola virus’ cell invasions triggered major upticks in the amount of calcium within the cells as they “hijacked” the signaling process.

Within the host cell, this action is controlled by a specific gene. By mutating this gene and placing it within the infected host cell, the calcium uptick was prevented. This also coincided with a dramatic fall in the production of Ebola virus by a factor of 100.

It must be noted that this technique's viability with human subjects remains questionable at this stage; calcium signaling is a crucial process within cells, and interrupting it would perhaps have detrimental knock-on effects within the body. Ronald Harty, one of the senior authors of the paper, told IFLScience: “[We would be] disrupting these host proteins for a short period of time (days/weeks)..as we would need to do to treat these acute (rapid) viral infections, [and this] would likely not have significant detrimental effects on the host because the treatment would not be long term.”

With some evidence suggesting that the natural reservoir for Ebola is more commonplace and far closer to humans than previously thought, this new research will hopefully contribute towards stemming the tide of deadly cases when the next outbreak occurs.

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