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Cold Sores Linked to Genetic Mutation

Update Date: Sep 16, 2013 03:24 PM EDT
cold sore, mouth, infection
Common infections can increase the risk of memory decline, according to a new study. (Photo : uiowa.edu)

Scientists have discovered why some people are troubled by cold sores.

A new study reveals that a mutation in a gene causes some people to be more prone to a strain of the herpes virus that causes cold sores.  This is because they have immune systems that are unable to prevent cold sores from developing.

Eighty to 90 percent of people are infected with the herpes simplex virus type 1 (HSV-1).  However, only about a quarter of these people get frequent cold sores.

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After analyzing thousands of genes, researchers from the University of Edinburgh were able to identify the ones that expressed the proteins needed for the immune system to prevent the virus from becoming active. Cold sores develop when the virus becomes active.

Afterwards, researchers looked at blood samples from people with cold sores. They found that one of the genes identified, the IL28b, was mutated in these people. Researchers explain that people with the mutation are more prone to cold sores because they have bodies that are unable to mount adequate immune responses to the virus.

Researchers also linked the IL28b gene to treatment responses for hepatitis C patients. Researchers found that patients are less likely to respond well to treatment if this gene is mutated. Researchers said the latest study supports previous findings that a single genetic mutation can be linked to different viruses.

"Most people carry the cold sore strain of the herpes simplex virus, but until now we never knew why only some of them develop cold sores," researcher Professor Juergen Haas, of the University of Edinburgh's Division of Pathway Medicine, said in a news release.

"Knowing that susceptibility to the virus involved relates to people's genes reinforces the need to research, not only the evolution of viruses themselves, but also the susceptibility of hosts to infection," Haas added.

The findings are published in the journal PLOS Pathogens

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