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Since the earliest days of the experiments, the Jerome team learned to rely on a cutting enzyme called a “meganuclease” that can zero in on a segment of herpes DNA and cut both strands of the double helix. “It gets us closer to really considering this as a curative approach. “It’s been three or four years of work, but I think what we describe in the paper is a really big step,” said Aubert.

Second, they chose different strains of harmless carrier viruses that do a better job of transporting those cutting tools to the places in the body where infected nerve cells are clustered. The more cuts these molecular scissors make, the harder it is for the virus to recover. First, the researchers added combinations of different gene-cutting enzymes.

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The advances in herpes cure research over the past five years are largely due to a series of improvements in the gene editing tools. Improvements in gene-editing tools - and patience - keys to success The first step will be to repeat their experiments using HSV-2 in guinea pigs, which, unlike mice, experience natural reactivations of herpes virus infections, just as humans do. The Jerome Lab’s herpes research thus far involves only HSV-1, but the scientists are now working on ways to extend their success to HSV-2. HSV-2 infection not only complicates the sex lives of couples, it also increases a person’s susceptibility to HIV, the virus that causes AIDS. Less than 1% of teens in the United States are infected, but that increases to 21% of Americans in their 40s, according to the Centers for Disease Control and Prevention. The prevalence of this chronic disease increases with age. According to the World Health Organization, two-thirds of the world population under the age of 50 carry herpes simplex virus type 1, or HSV-1, which primarily causes cold sores, while 491 million people aged 15-49 are infected with closely related HSV-2, which is the cause of sexually transmitted genital herpes.Īlthough the antiviral drug acyclovir can knock down an outbreak of HSV-2, the virus lingers for a lifetime within infected nerve cells and may reactivate, causing recurrent bouts of painful sores, on average, two to seven times per year. Herpes simplex viruses afflict billions of human beings around the globe. Jerome estimates that will be at least three years away. It will still take a long time before these experiments lead to the first human trials of gene therapy to cure herpes. “I hope that this study changes the dialogue around herpes research and opens up the idea that we can start thinking about cure, rather than just control of the virus,” Jerome said. Whereas most research on herpes has focused on suppressing the recurrence of painful symptoms, the Fred Hutch gene therapy work addresses the root cause of reactivation: the presence of latent virus in infected nerve cells.

Much of the team’s meticulous work of the past five years has involved finding better ways to target infected clusters of nerve cells and to thwart the virus’s ability to quickly repair the cuts to its genes. The hidden herpes viruses are disabled by an injection that tracks down infected nerve cells and induces them to make special gene-cutting enzymes, which work like a molecular scissors, to slash viral genes in specific places. “It is a completely different approach to herpes therapy than anybody’s ever had before.” “This is the first time that anybody has been able to go in and actually eliminate most of herpes in a body,” said Jerome, who is also spearheading research at Fred Hutch and the University of Washington on COVID-19. 18, the team led by Jerome and Aubert published a paper in Nature Communications showing that, through a series of incremental improvements on their original method, they had destroyed up to 95% of herpes virus lurking in certain nerve clusters of mice.

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