Now that researchers have located how cold sores operate , they think they may possibly quickly discover how to eradicate the virus that causes them. Cold sores, which usually show up as painful, ulcerated blemishes around the mouth, are triggered by the herpes simplex virus (HSV1). The virus frequently lies dormant in a nerve in the face, called the trigeminal nerve, till activated by sunlight, a poorly functioning immune technique, stressful situations or a higher fever.
By examining the interplay of various molecular substances the virus produces, researchers at Duke University Medical Center in Durham, N.C., have found how it hides and then emerges periodically. One particular such substance is named latency connected transcript RNA, which the study reveals blocks the formation of proteins that “turn” on the virus and make it replicate. It does this by splitting into strands of microRNAs, which primarily preserve the virus in check.
Nevertheless, in stressful conditions, the virus tends to make much more messenger RNA than the microRNAs can handle and ultimately viral replication happens. “We have offered a molecular understanding of how HSV1 hides and then switches back and forth among the latent [hidden] and active phases,” Bryan Cullen, Duke professor of molecular genetics and microbiology, mentioned in a release.
The researchers believe this discovery could lead to a therapy in which the artificial activation of the virus would lead it to be killed by administering acyclovir, a medication that kills replicating HSV1. The virus cannot be treated although in a dormant state. “In principle, you could activate and then kill all of the virus in a patient,” stated Cullen. “This would fully cure a person, and you would by no means get yet another cold sore .” The study is published in the June problem of the journal Nature.
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