A new finding that explains how hepatitis C virus (HCV) evades the destructive effects of interferon could lead to more effective therapies against the potentially fatal infection.
In the July 2 Science, Michael Lai, MD, PhD, of the University of Southern California School of Medicine, and his research team report that a protein component on HCV's envelope uses a kind of bait-and-switch tactic that allows the virus to survive.
As interferon binds to receptors on HCV-infected liver cells, production of protein kinase (PRK) causes phosphorylation of key proteins, which results in cell death and the demise of HCV. But the protein component on HCV's envelope, known as E2, mimics PRK's protein targets. When PRK binds to E2 instead of its normal targets, phosphorylation is inhibited and the virus lives on.
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