Everyone’s got herpes.

Between HHV-8, a lethal, cancer-causing strain of the virus and HHV-6, a relatively benign incarnation that rarely causes more than a fever, essentially all human beings are infected with some form of herpes. While the occasional cold sore may not perturb most patients, however, new research suggests that some medications activate herpes viruses, with potentially grave consequences.

Herpes, like many viruses, has a characteristic latency period during which the pathogen is barely detectable and causes no symptoms. When activated, however, herpes can rampage about the body, leaving painful sores in its wake. Researchers have long suspected that certain chemotherapy treatments, especially those that suppress the immune system, may activate latent herpes viruses even as the drugs carry out lifesaving tasks within the body.

“Viral reactivation during immunosuppressive therapy, especially chemotherapy, is a very real event,” said Dr. Jack Goldberg, oncologist at Penn Presbyterian Medical Center in Philadelphia.

In a new study published in Journal of Virology, a team of researchers at George Washington University (GWU) in Washington, D.C., found that prednisone, doxorubicin and vincristine, three immunosuppressive chemotherapy drugs also used in managing bone marrow transplants and severe allergies, are capable of activating some of the most common herpes viruses.

The offending drugs work by inducing programmed cell death, a normal cellular function called apoptosis, to destroy cancerous cells. Herpes viruses lying dormant within these doomed cells “sense” the impending death of their hosts and reactivate to infect new, healthy cells, said Dr. Steven Zeichner, a professor of medicine at GWU and coauthor of the study. “We now have considerably more support for the idea that herpes viruses can sense when their host cells are undergoing apoptosis,” he said. As a result, the viruses begin to replicate and produce symptoms that may be fatal, especially in cases of severe immunosuppression.

Despite these viral side effects, clinicians like Goldberg balk at the thought of discarding effective cancer treatments. “If you’ve got a drug that works, you’re going to find a way to use it,” he said. In that spirit, physicians have already begun prescribing antiviral treatments along with some cancer drugs in an effort to stave off viral reactivation.

Zeichner is enthusiastic about using precautionary anti-herpes drugs in a similar way, but cautions that plenty of clinical trials lie ahead. “Scientists hate to make absolutist statements until they have proved something about twenty different ways,” he said.

But Zeichner estimates that some strains of herpes infect the entire human population—potentially exposing millions of weakened patients to severe viral infections.

And with herpes hiding in us all, learning to tiptoe around the sleeping virus is an immediate priority.