Researchers from Tufts University and the University of Oxford have found that two common viruses—the varicella‑zoster virus and herpes simplex virus—may help trigger Alzheimer’s disease.

Varicella zoster (VZV), which causes chickenpox, often becomes dormant in peripheral nerves after infection. When reactivated, it causes shingles. HSV‑1, a subtype of the herpes simplex virus, causes oral and genital herpes and infects nearly 4 billion people worldwide under age 50. In the U.S., about half of all adults have oral herpes.

Cytokines—small proteins that regulate immune activity—are produced in response to VZV. While cytokines help immune cells do their job, excessive cytokine release can trigger an inflammatory overreaction known as a cytokine storm.

In findings published in the Journal of Alzheimer’s Disease, researchers showed that VZV infection of neurons triggers an inflammatory response driven by cytokine overproduction. This inflammation reactivates dormant HSV‑1 in the brain. With both viruses active, inflammation increases, potentially leading to plaque formation and the slow death of neurons—hallmarks of Alzheimer’s disease.

To study this, lead author Dana Cairns and colleagues used lab‑grown neural stem cell cultures. They found that VZV infection alone did not create Alzheimer‑like changes. However, when HSV‑1 was already present, VZV set off a cascade that produced plaques, tangled fibers, and neuronal damage.

“It’s a one‑two punch,” Cairns said. “These viruses are common and usually harmless. However, if VZV reawakens dormant HSV‑1, they can cause trouble.”

Oxford researcher Ruth Itzhaki, a pioneer in linking herpes infections to Alzheimer’s, contributed to the study.

The California Institute for Regenerative Medicine has invested nearly $35 million across 21 Alzheimer’s‑related projects. Under Proposition 14, CIRM is committed to investing at least $1.5 billion in treatments targeting the brain and central nervous system, including Alzheimer’s.