With over half the U.S. population infected, most people are familiar with the pesky cold sore outbreaks caused by the herpes simplex 1 virus. The virus outsmarts the immune system by interfering with the process that normally allows immune cells to recognize and destroy foreign invaders. How exactly the herpes simplex 1 virus pulls off its nifty scheme has long been elusive to scientists. Now, new research from The Rockefeller University sheds light on the phenomenon. A team of structural biologists in Dr. Jue Chen's Laboratory of Membrane Biology and Biophysics has captured atomic images of the virus in action, revealing how a viral protein (ICP47) is inserted into a key cellular protein to cause a traffic jam in an important immune system pathway. The findings were published online in Nature on January 20, 2016. The article is titled “A Mechanism of Viral Immune Evasion Revealed by Cryo-EM Analysis of the TAP Transporter.” "This work illustrates a striking example of how a persistent virus evades the immune system," says Dr. Chen. "Once this virus enters the body, it never leaves. Our findings provide a mechanistic explanation for how it's able to escape detection by immune cells." When a virus enters the body, it typically gets chewed up inside cells, and little pieces of the virus end up stuck to the outside of the cells. "These pieces act like a barcode to immune cells, which sense that a pathogen is present, and attack," says senior research associate and first author of the paper, Dr. Michael Oldham. One piece of the machinery involved in getting bits of virus to the cell's surface is a protein called TAP (transporter associated with antigen processing).
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