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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.
OverviewHerpes simplex, a common viral disease, is caused by two strains of the herpes simplex virus (HSV). The initial infection (primary stage) of oral herpes is generally asymptomatic and is acquired through person to person contact such as kissing. The stages of genital herpes are very similar to oral herpes with an initial stage that manifests with few symptoms and is less contagious.
For both genital and oral herpes, the dormancy period involves the virus "resting" within the nervous tissue around the initially infected area. Herpes is commonly diagnosed based upon the symptoms described above paired with frequent recurrence in the same area. Once diagnosed with herpes, managing the disease includes caring for sores during outbreaks as well as preventing their recurrence. Since genital and oral herpes are extremely common in the United States, with an estimate of 45 million people or one out of every five infected, there are many places to turn for support. Viral infections or exacerbations are still the most difficult problem in medicine to date.
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. Long-term prophylaxis of cold sores is indicated when you get cold sores frequently, at a rate of about 6 or more times per year.


Sex frequency in relationships can influence overall feelings about a partner and the relationship. All rights reserved.Medical Daily is for informational purposes and should not be considered medical advice, diagnosis or treatment recommendation. 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. The potential side effects of daily oral medication must be considered with infrequent cold sores. 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. In some instances, samples of representative lesions are taken and tested for the presence of the HSV1 or HSV2 virus.


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The virus lives in the nerve cells within the affected skin area, and when the immune system is weakened by stress or lack of sleep, an eruption can occur. When a person has an outbreak, the virus can be highly transmissible, and affected people are advised to avoid sexual contact."This is the beginning of an exciting period for our herpes vaccine. The drug works by blocking the virus from replicating and does not cure the infection, but can stop it in its tracks, force an outbreak to end, and allow healing.
Abreva is also sold as a treatment for cold sores, yet its effectiveness has been in dispute and has only been shown to lessen an outbreak by less than a day. Other research has suggested forcing an outbreak and treating with currently available medications, but this is still in the pre-clinical testing stages.Genital herpes affects more than one in six Americans between the ages of 14 and 49, according to the Centers for Disease Control and Prevention (CDC). Herpes outbreaks make people more susceptible to contracting other sexually transmitted infections (STIs) and increase the risk of HIV infection. Phase I trials usually use doses of drugs or vaccines that are meant to test the safe dosing range and may confer protection to those who participate in the trial.A previous vaccine tested by GlaxoSmithKline flopped in late-stage clinical trials, wasting 20 years and $100 million's worth of research money.



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  • killer_girl, 16.05.2015 at 13:59:50
    With herpes simplex virus kind 2 (HSV-2); nonetheless skin's surface is surrounded.
  • VASIF, 16.05.2015 at 15:51:59
    Quickly as prodromal (warning) signs indicating a recurrence are skilled herpes.
  • AYSEN_RAZIN, 16.05.2015 at 13:27:36
    Once-weekly drug dose have been one else could and neither could.