Skin

04 December 2008

Say goodbye to cold sores

Cold sores may be a thing of the past as researchers claim to have figured out what triggers the virus - and this may lead to a drug which can kill it.

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Cold sores, the painful blemishes of the mouth caused by the herpes simplex virus, may become a thing of the past, US researchers reported on Wednesday in the British weekly journal Nature.

They said they had uncovered a stealth mechanism that enables the virus to hide away in facial nerves before it is revived by a trigger such as excessive sunlight or fever.

The virus, known by its initials as HSV1, can hole up for years, out of reach of any drug, before being roused from dormancy. When it revives, it prompts a sore to return to the same location on the mouth as before.

A team led by Bryan Cullen, a professor of molecular genetics and microbiology at Duke University Medical Center in Durham, North Carolina, explored how HSV1 is able to switch between these latent and active phases.

’Sleeping’ virus holds the answer
They found that the answer lies in the sole product made by the virus during its slumber - strands of genetic material called LAT ribonucleic acid (RNA). During the period of dormancy, LAT RNA is chopped up into smaller strands, called micro-RNAs, which block the proteins that switch on the virus' replication machinery.

The wakeup call causes the virus to start producing lots of information-carrying strands called messenger RNAs. These overwhelm the micro-RNAs and eventually cause the replication machine to crank back into life.

The new supply of viruses then heads down the trigeminal nerve - the nerve that runs down the side of the cheek and provides facial sensation - to the site of the initial infection at the mouth.

In a press release, Cullen said the discovery threw up the prospect of drugs that would activate the virus and then kill it.

Activation is an essential step, as a dormant virus is untouchable. A new drug, currently being tested on lab animals, aims to interfere with the micro-RNAs that keep the virus de-activated.

Findings could hold hope for shingles sufferers
Once the virus is reawakened, the patient could take acyclovir, a proven drug against HSV1, Cullen hoped.

"In principle, you could activate and then kill the entire virus in a patient," said Cullen. "This would completely cure a person, and you would never get another cold sore."

The findings may also be useful in combating HSV-2, which causes painful genital sores, and chicken pox virus, which can return later in life as shingles. – (Sapa)

July 2008

Read more:
Cold sores, Alzheimer's link
Cold sore virus vs. cancer

 

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Dr Suretha Kannenberg holds a degree in Medicine and a Masters in Dermatology from the University of Stellenbosch. She is employed as a consultant dermatologist by Stellenbosch University and Tygerberg Academic Hospital, where she is involved in clinical duties and the training of medical students and dermatology residents. Her areas of interest and research include vitiligo, eczema and acne. She also performs limited private practice work in the Northern suburbs of Cape Town in general and cosmetic dermatology.

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