A virus carried by more than 60 percent of people worldwide may alter the brain’s immune system in a way that could help explain a long-suspected link to Alzheimer’s disease, a new study suggests.
University of Colorado Anschutz scientists have discovered that herpes simplex virus type 1 (HSV-1), the virus that causes cold sores, can reshape the behavior of microglia, the brain’s primary immune cells. Their findings, published in PLOS Pathogenssuggest that although these cells develop a strong defense against infection, they may simultaneously lose some of their normal protective functions that help keep the brain healthy.
Dr. Kimberley Bruce, associate professor of medicine at CU Anschutz and co-senior author of the study, said News week What was particularly intriguing was how immune cells exposed to the virus resembled cells associated with major genetic risk factors for Alzheimer’s disease.
“What we find very interesting is that the way innate immune cells in the brain respond to the virus makes them behave similarly to cells that carry certain major genetic risk factors, such as ApoE4,” Bruce said. “These cells express a lot of interferons, the antiviral machinery.
“So one of the things we hope to explore is whether specific factors that target this interferon pathway can improve cellular function without losing immune competence, to perhaps reduce the risk (of Alzheimer’s disease) a little bit.”
Dr. Christy Niemeyer, assistant professor in the department of neurology at the college’s medical school and lead author of the study, also spoke with News week on the results.
“As Dr. Bruce mentioned, we are also interested in the bigger picture: Alzheimer’s disease is a complex disease with many genetic and environmental risk factors, and these factors do not exist in isolation. Could these risk factors work together to make the brain more vulnerable to the disease?” » said Niemeyer. “Ultimately, we hope to better understand how these different risk factors interact and whether we can find ways to reduce harmful inflammation while still allowing the brain’s immune cells to do their job.”
How the virus changes the brain’s immune cells
Research has focused on understanding how HSV-1 influences microglia after infection. These specialized immune cells normally help maintain a healthy brain by clearing debris, supporting neurons, and regulating inflammation.
Researchers found that once HSV-1 infects the brain, microglia shift to a highly activated, antiviral state. This response is driven by interferons, molecules that play a central role in the fight against viruses.
However, the transition comes with compromises. As microglia focus on fighting new infections, genes related to their normal maintenance and protective functions become less active and less concentrated.
Using advanced molecular techniques, researchers analyzed how individual brain cells responded to HSV-1 infection. They identified distinct populations of microglia dominated by interferon signaling while discovering a reduction in the activity of genes associated with routine brain maintenance.
The changes were concentrated in regions where the virus was detected, suggesting that HSV-1 creates localized pockets of increased immune activity in the brain.
The team also observed alterations in chromatin, the material that packages DNA inside cells. Such changes can influence how easily genes are turned on or off, potentially affecting cellular behavior over time.
Possible connection with Alzheimer’s disease
Alzheimer’s disease is influenced by a complex mix of genetic and environmental factors, and scientists are increasingly studying whether common viral infections may contribute to disease processes.
HSV-1 remains in the body for life after infection. Although serious complications are rare, growing evidence links the virus to chronic inflammation, a process thought to play a role in Alzheimer’s disease. However, until now, the biological mechanisms linking the virus to long-term brain inflammation remain unclear.
The new findings offer a possible explanation by showing how infection can push microglia into a prolonged antiviral state while reducing their ability to perform functions important for brain health.
The researchers now plan to examine whether these immune changes continue after the infection clears and whether repeated viral reactivation could have lasting effects on the brain.
Neurologist Dr Hanul Bhandari, senior consultant at New Waters Recovery, said the study provides insight into how HSV-1 can influence brain biology, but does not prove that the virus causes Alzheimer’s disease.
“I consider the main advance to be the study’s ability to map where and how microglia change after herpes simplex virus type 1 infection,” Bhandari said. News week. “These results clarify a potential biological pathway, but they do not establish that HSV-1 causes Alzheimer’s disease.”
He noted that the brain needs a carefully balanced immune response to control viral infections without harming neurons and that scientists still don’t know whether virus-related immune changes persist long enough to trigger neurodegeneration.
“Herpes viruses may be involved in the pathogenesis of Alzheimer’s disease,” he said. “However, being a carrier of these common viruses in no way guarantees that you will get Alzheimer’s disease or another form of dementia.”
Reference
Niemeye, C.S., Bruce, K.D. (2026). Intranasal HSV‑1 infection results in region-specific interferon-dominant microglial remodeling. PLOS Pathogens. https://doi.org/10.1371/journal.ppat.1014684.
Contact Newsweek editors about this story: Kara Dolman And Paul Donnelley.
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