Scientists may have finally found a way to wipe out the herpes virus for good, putting an end to recurring skin conditions such as cold sores, genital herpes and shingles.
Researchers at Duke University in North Carolina, reported this month in the journal Nature that they have discovered a gene carried by the herpes simplex-1 virus allows the virus to lay dormant in the nerves under the surface of the skin. It does so via microRNAs, little pieces of genetic material that regulate the activity of many viruses, the researchers report in the journal Nature. The researchers found that it may be possible to "wake up" the virus and then kill it with standard antiviral drugs. Herpes viruses cause permanent infections. They lie dormant in nerve cells below the skin’s surface and cause periodic outbreaks. Herpes simplex 1 or HSV-1 causes cold sores, HSV-2 causes genital herpes, while varicella causes chicken pox and returns in middle or old age as herpes zoster, causing shingles. All types of herpes virus are impossible to kill with current medications because the virus is only vulnerable when it is active and it’s impossible to predict when it will be active or where in the body.
However the researchers found that a gene called LAT controls microRNAs that turn off other genes in the virus. The presence of these active microRNAs keeps the virus dormant. When the virus is activated by stress like UV (ultraviolet) light or a wound, production of (other) genes goes up. Then LAT is overwhelmed and unable to keep the virus in check. It wakes up and causes an outbreak.
But, the researchers said, a drug that turns off the microRNAs could drive the virus out of hiding and allow all copies of the virus to be killed easily with anti-viral medication. The researchers suggested that one class of drug called an antagomir might work. These chemically engineered oligonucleotides are short segments of RNA that can be made into mirror images of a targeted bit of genetic material -- such as the herpes microRNAs. They would effectively attach and "silence" the microRNA.
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