Researchers Identify Disabling Protein that can Stop the Ebola Virus
Researchers from the University of Texas at Austin are collaborating with Mount Sinai Hospital in New York to help identify key vulnerabilities in the deadly ebola virus. the effort, which is led by Dr. Christopher Basler, PhD, Associate Professor of Microbiology at Mount Sinai and his team from the Icahn School of Medicine, have already uncovered key data about how disabling a protein in ebola virus cells can halt the virus in its tracks, thus stopping it from replicating and infecting whomever has been exposed and afflicted with the virus. The data was recently published in the July edition of the journal Cell Host and Microbe.
Dr. Basler reveals that ebola viruses are particularly deadly because they can essentially shut down a person’s innate immune system. The deactiviation of the immune system is caused by the viral protein VP35. When VP35 interacts with a critical cellular protein known as PACT, it stops PACT from turning on the immune system. By doing so, this is precisely what allows a virus like ebola to spread quickly throughout the body.
Dr. Basler explains that, “Ebola viruses are extremely lethal, and are a great threat to human health as a bioweapon. Currently, there is no approved vaccine or treatment. Our findings will hopefully pave the way for future antiviral treatments.”
In order to effectively experiment with how this interaction can be disrupted, UT researchers leveraged their special high containment facilities to infect healthy cells with Ebola virus cells that had mutated versions of VP35. According to an article on Eureka Alert, “the mutations disabled VP35′s ability to interact with PACT, therefore allowing it to activate the immune system and prevent the virus from replicating. Next, the researchers overexpressed PACT in healthy cells, and infected them with Ebola virus cells. They found that overexpressing PACT also inhibited viral replication.”
The next step will be to use this discovery to determine means by which this interaction be disrupted, or a means to overexpress PACT so that the deactivation of the immune system is thus neutralized.
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