Shutting down this pathway foiled the virus’ ability to fully infect cells and reproduce, according to study in PloS Pathogens.

Researchers from University of Texas Medical Branch at Galveston (UTMB) discovered that the Ebola Zaire virus uses the phophoinositide-3 (PI3) kinase pathway to infect cells. They also found that once this pathway is shut down, the disease process gets halted.

The scientists found that the Ebola Zaire virus activates the P13 kinase pathway, tricking the cell into pulling the virus into the cell’s endosome. This endosome along with the virus is then drawn into the cell. Once inside the cell, at a critical point the virus bursts free from the endosome and begins to reproduce itself.

The investigators then developed a compound designed to block the P13 kinase pathway. They observed that the virus particles could then no longer escape from the endosome, essentially stopping infection.

The team worked with the Ebola Zaire virus as well as harmless, hollow, virus-like particles coated with the critical envelope proteins that activate the PI3 kinase pathway. Using a test created at UTMB that adds the light-emitting molecular beacon liciferase to Ebola viruses and the virus-like particles, the investigators were able to determine exactly when and where each virus broke out of its bubble and track its progress.

While other viruses that activate the PI3 kinase pathway have been found, Ebola is the first with envelope proteins, according to Robert Davey, Ph.D., associate professor of microbiology and immunology and senior author of the paper. In addition, it was the first virus to be discovered interacting with the PI3 kinase pathway to enter cells, he adds.

The study appears online in PloS Pathogens.

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