White fat cells can be turned into energy-burning brown fat using CRISPR gene-editing technology. These engineered cells have helped mice avoid weight gain and diabetes when on a high-fat diet, and could eventually be used to treat obesity-related disorders, say the researchers behind the work.

Human adults have plenty of white fat, the cells filled with lipid that make up fatty deposits. But we have much smaller reserves of brown fat cells, which burn energy as well as storing it. People typically lose brown fat as they age or put on weight. While brown fat seems to be stimulated when we are exposed to cold temperatures, there are no established methods of building up brown fat in the body.

Researchers at the Fred Hutchinson Cancer Research Center in Seattle, USA, have used gene editing to remove latent herpes simplex virus 1 (HSV-1), also known as oral herpes.

In mice, the technique showed a 92% decrease in the latent virus – enough to keep the infection from coming back, according to the scientists. The study used two sets of “genetic scissors” to damage the virus’s DNA, fine-tune a delivery vehicle to the infected cells, and target the nerve pathways connecting the neck with the face, reaching the tissue where the virus lies dormant. The findings are published in Nature Communications.

“This is the first time that scientists have been able to go in and actually eliminate most of the herpes in a body,” said senior author Dr. Keith Jerome, Professor in the Vaccine and Infectious Disease Division at Fred Hutch. “We are targeting the root cause of the infection: the infected cells where the virus lies dormant and are the seeds that give rise to repeat infections.”

Biologists often speak of switching genes on and off to give microbes new abilities–like producing biofuels or drugs, or gobbling up environmental toxins. For the most part, though, it’s nearly impossible to turn off a gene without deleting it (which means you can’t turn it on again). This limits biologists’ ability to control how much of a particular protein a microbe produces. It also restricts bioengineers’ ability to design new microbes.

Now researchers at Boston University, led by biomedical engineering professor James Collins, have developed a highly tunable genetic “switch” that offers a greater degree of control over microbes. It makes it possible to stop the production of a protein and restart it again. The switch, which could be used to control any gene, can also act as a “dimmer switch” to finely tune how much protein a microbe would produce over time.

The researchers made a highly effective microbe “kill switch” to demonstrate the precision of the approach. For years, researchers have been trying to develop these self-destruction mechanisms to allay concerns that genetically engineered microbes might prove impossible to eradicate once they’ve outlived their usefulness. But previous kill switches haven’t offered tight enough control to pass governmental regulatory muster because it was difficult to make it turn on in all the cells in a population at the same time.