University of Pittsburgh

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Breakthroughs in the Making

Written by Ervin Dyer

From left: Kinchington, Knickelbein, and Hendricks

From left: Kinchington, Knickelbein, and Hendricks

The herpes simplex virus type 1 (HSV-1) is like a lion at rest. Asleep, it’s harmless, but when awakened, it’s a threat. New research at the University of Pittsburgh shows that the immune system constantly monitors the virus, which can lurk for a lifetime in the body’s nerve cells once the initial infection occurs. This challenges the old notion that, when dormant in nerve cells, the virus is invisible to the immune system.

Nine of 10 people carry HSV-1, and when the virus goes on the prowl it usually causes only an occasional cold sore. But it can become more harmful to health, even leading to blindness or encephalitis, especially in those with weakened immune responses.

Typically, to destroy a virus, the immune system kills the cells that contain the virus, leaving only the healthy cells to replicate and restore function. But HSV-1 infiltrates sensory nerve cells, which may not replicate. In pursuit of a way to stop HSV-1, scientists have been reluctant to risk destroying sensory neurons.

Now, though, researchers at Pitt have found a key to stopping the virus. Their discovery sheds light on how the immune system keeps HSV-1 in check. Robert Hendricks and Paul R. Kinchington, both professors in the School of Medicine, led research endeavors which showed that particular immune cells, known as CD8 T cells, can send toxic enzymes into the nerve cells, removing a protein that promotes HSV-1 replication.Their results, published with lead author Jared Knickelbein and other coauthors last fall in the prestigious journal Science, also suggest that the virus only becomes active if the biological balance shifts and the immune cells don’t effectively stop HSV-1 replication.

There is no cure for herpes, but by keeping HSV-1 infections in check, researchers hope to slow outbreaks of cold sores and other illnesses, including perhaps genital herpes, which is caused by another strain of the virus.