Researchers from the Salk Institute announced on Wednesday that they have discovered the mechanism viruses like West Nile and dengue use to shut down the body's defense system.
The findings showed a mechanism that a group of viruses use to disarm the host body's immune response. The viruses activate a class of molecules, called TAM receptors, located on some immune cells by using a substance called phosphatidylserine, which binds to extracellular proteins and activates TAM receptors on immune cells.
"Our findings suggest a unique way in which TAM receptors contribute to the establishment of viral infection by disabling the interferon response," John A.T. Young, a professor in Salk's Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis and co-lead study author, said. "As a consequence, the interferon-stimulated defense genes are not turned on, rendering the target cell more permissive for virus infection."
The researchers also looked at ways to counter the viruses' ability to shut down the interferon response in cells. They found that a small-molecule drug called BMS-777607, which was initially developed for anti-cancer therapy, is capable of shutting down interferon response in cells by blocking TAM receptor activation.
"With this small molecule, viruses can't activate TAM receptors, so they can't shut down the interferon response," Greg Lemke, a professor in Salk's Molecular Neurobiology Laboratory and co-lead author, said.
The study was published in the August issue of the journal Cell Host and Microbe.