Great resource for information on herpes and how to treat and cure herpes.

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Cure For Herpes

Sexually transmitted infections hit a new record last year. The total increased by 6 per cent in 2007 to 397,990 new cases.

Pequeños fragmentos del genoma humano son los causantes de que el virus del herpes pueda sobrevivir durante años en estado de latencia en las neuronas, según descubrieron científicos estadunidenses del Centro Médico Universitario Duke en Durham, de Carolina del Norte. En ese estadio, que los expertos califican de infección latente o dormida, los virus no son susceptibles a los medicamentos, indicaron los investigadores encabezados por Bryan Cullen en un artículo publicado en la revista británica Nature, en su versión online. Los fragmentos del genoma analizados evitan la formación de proteínas necesarias para despertar a los virus. Los investigadores esperan utilizar los resultados de sus investigaciones para desarrollar una forma de sacar de la latencia a los virus, con el propósito de que sean susceptibles a los medicamentos antivirales.

Now that Duke University Medical Center scientists have figured out how the virus that causes cold sores hides out, they may have a way to wake it up and kill it. Cold sores, painful, unsightly blemishes around the mouth, have so far evaded a cure or even prevention. They're known to be caused by the herpes simplex virus 1 (HSV1), which lies dormant in the trigeminal nerve of the face until triggered to reawaken by excessive sunlight, fever, or other stresses. "We have provided a molecular understanding of how HSV1 hides and then switches back and forth between the latent (hidden) and active phases," said Bryan Cullen, Duke professor of molecular genetics and microbiology ... Most of the time, HSV1 lives quietly for years, out of reach of any therapy we have against it. It does not replicate itself during this time and only produces one molecular product, called latency associated transcript RNA or LAT RNA. "It has always been a mystery what this product, LAT RNA, does," Cullen said. "Usually viral RNAs exist to make proteins that are of use to the virus, but this LAT RNA is extremely unstable and does not make any proteins." In studies of mice, the team showed that the LAT RNA is processed into smaller strands, called microRNAs, that block production of the proteins that make the virus turn on active replication. As long as the supply of microRNAs is sufficient, the virus stays dormant.

Millions are affected with the painful blemishes around the mouth and, although there is an effective treatment, the virus is able to go into hiding and then launch another attack, notably when a person is run down and exhausted. advertisement Now scientists have found out how the cold sore virus hides and are testing a way to smoke it out, so that it can be eradicated, an approach that could be extended to other latent infections, such as shingles and genital herpes. Duke University Medical Centre scientists studied how the herpes simplex virus 1 is able to lie dormant in the trigeminal nerve of the face until triggered to reawaken by excessive sunlight, fever, or other stresses. "We have provided a molecular understanding of how HSV1 hides," said Prof Bryan Cullen of Duke, one of the team that reports the study in Nature. The team focused on the one sign of a latent infection by the virus, when it is out of the reach of treatments, the production of a molecule called latency associated transcript RNA or LAT RNA.