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Gene May Help Herpes Virus Enter Cells

Newly Found Gene May Be the Gatekeeper for the Virus
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WebMD Health News

July 25, 2005 -- When the herpes virus enters a cell, it may not have to blast its way into cells. A newly discovered gene may put out the welcome mat for the virus.

If so, it might one day be possible to thwart the virus by slamming that door shut.

Scientists are just starting to learn about the gene, called hfl-B5, and its effects. They watched the gene and virus in lab tests on human and pig cells. The results appear in the Journal of Virology.

About the Virus

The herpes simplex virus comes in two forms: HSV1 and HSV2. They can cause small, painful, blister-like sores of the skin or the tissue lining of the throat, nose, mouth, urethra, rectum, and vagina.

A herpes infection may cause only a single outbreak of sores, but the virus often flares up again later. Herpes can have severe effects on people with weak immune systems and those who are chronically ill or bedridden, the researchers note.

Herpes can be transmitted through sex. At least 45 million people aged 12 and older in the U.S. have had genital herpes infections. Most don't know they've had herpes, states the CDC's web site.

Gene to Virus: Come on In

The gene makes a protein called B5, which is found in cell membranes.

A cell's membrane is like a living, moveable wall around a city. It's supposed to protect the cell, letting helpful items in and waste products out, while keeping the bad guys at arm's length.

Along the membrane are all sorts of receptors that work like customs agents. The B5 protein appears to act as a receptor for the herpes simplex virus, the researchers write. When the herpes simplex virus -- definitely a bad guy -- sidled up to B5, the protein let the virus into the cell.

That's what A. Oveta Fuller, PhD, and colleagues found. Fuller is an associate professor in the microbiology and immunology department at the University of Michigan's medical school.

 

Closing the Door

In another test, Fuller and colleagues tinkered with part of the B5 protein in pig cells. That kept the herpes virus out, the researchers write.

In other words, when they changed the lock (the B5 protein), the old key (the herpes virus) couldn't open the door into the cell.

That particular spot on the B5 protein is "a potential new target to intervene in the virus infection of human cells," write the researchers.

 

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