A cold sore might seem like a minor nuisance. But behind that tingling lip is one of the world’s most widespread and cunning viruses—herpes simplex virus type 1, or HSV-1. It infects billions of people. You’re probably infected with it without even knowing it. And according to new research, the virus reshapes our DNA faster than anyone imagined.
Scientists in Spain and China discovered that HSV-1 begins rewriting the architecture of human genes just one hour after infection. It doesn’t just sneak in and make copies of itself; it takes over the cell’s genetic control room and reroutes it for its own needs.
A Fast Genetic Hacker
The herpes virus spreads easily through skin contact, saliva, or even by touching the area around someone’s mouth. Once inside the body, it heads for our cells — and in particular, the nucleus, where all our genetic instructions are stored.
There, HSV-1 does something remarkable. It diverts the tools our cells use to read DNA, pulling them away from our own genes and directing them to its own viral blueprint. These tools, especially a molecule called RNA polymerase II, are like factory workers that normally keep the cell running. When the virus steals them, our cells stop making many of their usual proteins. Instead, they start churning out materials for the virus.
This change happens fast. In just a few hours, the virus has rerouted most of the machinery to itself, turning the cell into a virus-making factory.
Your DNA, Hijacked
As HSV-1 takes control, it doesn’t just hijack our genetic machinery—it reshapes the very structure of our DNA in the infected cells.
Using ultra-precise microscopes, researchers watched as the virus caused the cell’s genetic material to collapse inward. Within eight hours, the host genome had shrunk to just 30% of its original volume. This was a direct result of the virus pulling essential proteins away from human DNA and redirecting them to its own.
The virus was found to make physical contact with specific regions of the human genome, particularly regions that remain active during infection. “We used to think it made contact with our genome randomly,” Esther González-Almela, a biologist at the Centre for Genomic Regulation, told New Scientist. “But the virus is able to contact our own genome in specific regions, and these regions usually harbour genes that are involved in the continuity of infection, in making viral RNA and proteins.”
What’s more, the researchers discovered that HSV-1 doesn’t just push the host cell into silence—it activates genes that are useful to the virus. Those genes become more active, helping the virus replicate and spread.
At the same time, most of the cell’s own transcription—the process of reading and expressing genes—slows dramatically. In fact, by eight hours after infection, human gene activity had dropped to less than 10% of the total transcription happening in the cell.
Could This Insight Lead to New Treatments?
The research team didn’t just watch the virus take over. They also tested a way to stop it.
In their experiments, the scientists used an experimental cancer drug to block TOP1, one of the transcription-related proteins that HSV-1 steals from human cells. When they did this in lab-grown human lung cells, the virus couldn’t replicate.
“This suggests that the drug could help treat HSV-1 in people with severe cold sores or those who have a suppressed immune system and are more likely to experience complications,” said González-Almela.
The implications could go beyond cold sores. The team notes that other viruses may rely on similar strategies to hijack human cells. “Other viruses similar to HSV-1 may use similar strategies,” said Benjamin Krishna, a virologist at the University of Cambridge. “There’s a possibility that these [sorts of experimental drugs] could treat those as well.”
For now, the findings offer a new window into how viruses manipulate the inner workings of human cells—and a potential starting point for developing treatments that cut off their power supply before they spread.
A Familiar Virus, a Hidden Danger
Herpes simplex virus 1 is incredibly common. It’s estimated that two-thirds of people worldwide carry it, even if they’ve never had symptoms. It often hides in nerve cells and reactivates from time to time, usually as cold sores.
But in people with compromised immune systems—like cancer patients or organ transplant recipients—it can cause more serious problems, including infections in the eyes or brain.
This research doesn’t just help us understand herpes. It shows how some viruses can bend the rules of our biology to take over, and how modern science is starting to catch them in the act.
The virus may have a head start. But for the first time, scientists are seeing its playbook in real time. And they’re learning how to fight back.
The study was published in Nature Communications.
