Researchers from the Scripps Research Institute claim to have uncovered the mechanism how viral infections inhibited the production of vital immune system proteins, opening up avenues for developing new treatments for HIV, measles, and tuberculosis.
The study showed how an initial viral infection can block production of critical immune system proteins known as type I interferons, which plays a range of roles including direct antiviral effects, activating innate natural killer cells and adaptive T lymphocytes, which destroy a wide range of infectious invaders.
"It’s the first demonstration that a virus causes suppression of the interferon response in vivo," said senior author Michael Oldstone, a Scripps Research professor and a pioneer in immune system studies.
"This model explains how a secondary infection can be caused by a normal virus infection and this provides the guide for what to do and where to look in human diseases, which are of course more difficult," he added.
The research team led by Elina Zuniga, formerly a postdoctoral fellow in the Oldstone lab, worked with mice infected with lymphocytic choriomeningitis virus.
They found that the virus suppressed the mouse immune system by interacting with immune cells known as plamacytoid dendritic cells, which are key producers of one of two critical groups of interferons, known as type I.
When plasmacytoid dendritic cells come in contact with viruses and other foreign invaders, they bind with them via membrane proteins known as toll-like receptors.
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