A protein may hold the key to halting the spread of genital herpes in the nervous system, a groundbreaking new study has claimed.
The findings may lead to improved treatment of the sexually-transmitted disease, according to University of Arizona College of Medicine-Phoenix researchers.
Experts said the protein, called IL-36y, goes into “hiding” once it enters the body and occasionally reactivates – causing lesions.
It plays an important role in chronic inflammatory diseases, but it was found that it could protect infected people.
Jameson Gardner, who led the study, said the virus spread through the nervous system in those with HSV-2 in those lacking IL-36y.
But, in those with the gene intact were more protected against the spread.
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The researcher continued: “The researchers really were excited to see that after intravaginal HSV-2 infection, the virus was able to spread systematically throughout the nervous system and to the brain in those lacking IL-36y.”
Mr Gardner added that a control group, which had the gene intact, was much more protected against HSV-2 spread in the nervous system.
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The graduate research student added: “We’ve shown that IL-36y appears to function in a previously-uncharted manner to protect against virus neuroinvasion (an infection that affects the nervous system.”
But, it isn’t yet known how IL-36y does this – according to the study’s authors.
While there are antiviral medications that treat genital herpes, there are some 260million women across the globe who have the life-long infection that can be transmitted to others.
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For decades, researchers have tried to find a cure to protect against the virus – none of which have been successful.
Gardner continued: “Our understanding of how IL-36y functions can aid in the development of novel therapeutics to protect against and hopefully decrease the burden of sexually transmitted infections around the world.”
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