I took a breath, let it out. I hate this part, I said to myself, possibly aloud. And then, definitely aloud: Go read the whole thing. Trust me. Right now.
Share Hutch News. Martine Aubert and Keith Jerome showed for the first time in a living organism that DNA-cutting enzymes called targeted endonucleases can be used to disrupt latent herpes simplex virus. Herpes researchers at Fred Hutchinson Cancer Research Center have used a gene-editing technique to attack the DNA of the herpes simplex virus in infected mice. This new research is a key step toward a cure for herpes, an often stigmatized virus that infects one in six people in the United States alone.
The study is the first in a living organism — rather than a lab dish — to show that gene-editing tools can be delivered to the herpes simplex virus in its latent state or to a latent viral infection of any kind. Doing so is key to curing herpes because a latent infection can reactivate and seed new outbreaks. There are two types of herpes simplex virus. The most widespread is herpes simplex virus 1, or HSV-1, which is usually transmitted through mouth-to-mouth contact.
During an active infection, HSV-1 can cause so-called cold sores around the lips. Globally, it infects more than 3. More troublesome is genital herpes, which is usually caused by herpes simplex 2, or HSV-2, and affects about million people, or about 11 percent, worldwide. It is transmitted through skin-to-skin contact during vaginal or anal sex and can cause painful genital and anal lesions. Another million people have genital lesions caused by HSV-1 transmitted through oral sex, bringing the total number of those with genital herpes to more than half a billion.
In people with suppressed immune systems, such as those undergoing chemotherapy or other cancer treatments, sores can be severe. Genital lesions also can increase the risk of transmitting or getting HIV. The U. Centers for Disease Control and Prevention states that , Americans are newly infected with genital herpes each year. Even when symptoms are nonexistent, mild or suppressed by medication, infected people can still spread the disease to their sexual partners, making a genital herpes diagnosis a source of embarrassment, shame or stress that can interfere with relationships.
It’s not like you can easily tell your friends and family of your new herpes diagnosis. HSV infections occur at mucosal surfaces — the mouth, the genitals. The virus is then picked up by sensory nerve endings on those surfaces and travels along axons to neuronal cell bodies, where it persists in a dormant state. But unlike some other lifelong infections that have latent stages — HIV, for example — dormant herpes simplex viruses rest in just two places in the body: Having these virus dormitories confined to such specific sites is a huge advantage for researchers seeking to cure herpes, as is the relatively small number of neurons infected.
She injected the instruction-carrying virus into the whisker pads of the mice, where it entered the nerves through a path similar to the one used by the herpesvirus, traveling through the axons to the nerve bodies where latent herpes resides. Measurable disruption of HSV occurred in a majority of the mice, but the amount of virus with genetic damage was low, 2 to 4 percent.
The goal now is to get more enzymes into the ganglia where they can act. The gene-editing platform used in the study is an older type known as a meganuclease. In , Science magazine named it the breakthrough of the year. Even partial results may help ease recurrent infections. Earlier studies have shown that the frequency and severity of lesions is related to how much virus is present in the ganglia. Eliminating just half of the latent infection could help ease recurrences from one every month to one or two a year.
Fred Hutch and UW have long been a hub of herpes research, largely thanks to the presence of Dr. Lots of us trained with him over the years. Today, acyclovir and its successors have reduced mortality rates for babies born with herpes from 80 to 10 percent. It is not a cure. Jerome started out studying the basic interactions between herpes and its host. Then about five years ago, he noticed the work that Fred Hutch structural biologist Dr.
Why would anybody want to be cured? An online survey of more than people with genital herpes found that up to 81 percent were interested in participating in clinical trials aimed at curing HSV — despite the availability of suppressive therapy. Are you interested in reprinting or republishing this story? Be our guest! We want to help connect people with the information they need.
Email us at communications fredhutch. Subscribe to RSS. Is it possible to prevent breast cancer metastasis? Could a simple blood test replace the invasive tissue biopsy? A new focus on small cell lung cancer. Magazine Archive Back issues of Hutch Magazine. Science Spotlight Monthly review of Center-authored papers. Home Hutch News Can gene editing cure herpes?
Can gene editing cure herpes? Similar stories. The ins and outs of gene editing and its potential for cures. The big 4 gene-editing platforms and how they could usher in new therapies for HIV, cancer — and other diseases. New Hutch study predicts threshold of viral load for passing herpes from one person to another. News releases Media coverage Find a researcher Contact us.
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