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admin 11.03.2015

By age 40, nearly 90% of adults have been exposed to the herpes simplex virus-1 (HSV-1), which causes cold sores.
Until now, research has generally concentrated on keeping HSV1 inactive — and preventing cold sores from ever showing up. Understanding how to override the microRNA could allow scientists to activate the virus and then kill it using acyclovir. The theory is that by activating the virus, then preventing it from returning to hibernation, which is when researchers think it gains strength, it can be completely eradicated. Cullen and his colleagues, as well as several biotech firms, are already investigating such treatments and how best to deliver them.
But when triggered by excessive sunlight, fever, or other stresses, it erupts into the painful, unsightly blemishes known as cold sores. But the Duke researchers took the opposite tack: figuring out precisely how to switch the virus from latency to its active stage.
Cullen believes that a drug could be developed to block the microRNA that suppress HSV-1 into latency; once it's active, acyclovir can be used to destroy the virus permanently. The virus is common but has evaded a cure and even efforts at prevention—so far, that is.Duke Medical Center scientists, supported by two National Institutes of Health grants, say they have figured out how the virus that causes cold sores hides out. For those who do, however, cold sores are a painful and permanent nuisance, always erupting in the same location, at the original site of infection on the lips or mouth.

In its latent stage, HSV-1 produces a single molecular product, called latency-associated transcript RNA, or LAT RNA.
Cullen suggests that this new research may also eventually be applied to other latent viruses, such as herpes simplex virus-2 (HSV-2), which causes genital herpes, or the chicken pox virus, which causes shingles in adults. They believe that this knowledge may yield important clues as to how to kill it.The first step is waking up the virus.
Worse yet, once you're infected with the virus that causes them, you're stuck with it for good.
Once HSV-1 enters the body it hunkers down for life, most of the time hiding dormant in the cranial nerves near the spine.
Unlike most messenger RNA, LAT RNA doesn't produce proteins, so scientists have never been able to determine LAT RNA's exact function. Cullen warns that some patients, especially those suffering genital herpes, may have to take acyclovir on a regular basis (HSV-2 is a hardier virus), but for people with HSV-1, the virus could be eradicated with just one dose. But landmark research reported today by microbiologists at Duke University may offer the potential for a cure. The virus can be triggered by outside stress, such as exposure to sunlight, a fever or emotional distress. But by inserting the LAT RNA into mice, Cullen found that it breaks down into even smaller strands called microRNA.

After it's active and a cold sore appears, it's treatable with the drug acyclovir, marketed under the name Zovirax, which kills replicating HSV-1.
Researchers then discovered that it was the microRNA that blocked production of the protein that activates HSV-1.
It produces only one molecular product, called "latency associated transcript RNA," or LAT RNA for short. But the mystery has been how to eliminate the virus while it's hiding, before it produces unsightly symptoms.
As long as the supply of microRNAs is sufficient, the virus stays dormant.This finding suggests that a combination therapy may be within reach, Cullen says. He and his team are testing a new drug designed to bind precisely to the microRNAs that keep the virus dormant. If it works, the virus would become activated and start replicating.Once the virus is active, a patient would then take acyclovir, a drug that effectively kills replicating HSV1.

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