According to new research led by the University of Colorado Anschutz, herpes simplex virus type 1 (HSV-1)—the virus responsible for cold sores—alters the structure of microglia in a specific region of the brainstem. It remains unknown, however, whether these changes persist long-term or if they influence the risk of developing Alzheimer’s disease. The findings were published in the journal PLoS Pathogens.
Herpes simplex virus type 1 (HSV-1) affects a significant portion of the global population, remaining dormant within nerve cells throughout a person’s lifetime.
While serious complications are rare, a growing body of evidence suggests a link between HSV-1 and chronic inflammation, which may potentially trigger Alzheimer’s disease.
However, it remains unclear exactly how the virus might initiate and sustain this inflammation.
“Microglia act as both the brain’s security system and its maintenance crew,” said study co-author Christy Niemeyer of the University of Colorado Anschutz. “When HSV-1 enters the brain, these cells shift into an emergency defense mode. While this helps fight the virus, it can also compromise their ability to carry out routine, day-to-day functions—even after the virus is gone.”
In the study, researchers infected mice with a strain of HSV-1 and subsequently examined their brains six days later—a point the researchers describe as the peak of the innate immune response. Using advanced molecular techniques, the researchers studied how individual brain cells respond to an infection with herpes simplex virus type 1 (HSV-1) and precisely where these changes occur.
They discovered that the infection leads to the emergence of distinct populations of microglia—a type of immune cell in the brain—characterized by heightened interferon signaling, a potent antiviral defense mechanism.
Concurrently, there was a decrease in the activity of genes involved in the cells’ normal protective and supportive functions.
Significantly, these changes were concentrated in the specific brain regions where the virus was detected, suggesting that HSV-1 creates localized zones of intensified immune activity.
The researchers also observed alterations in chromatin—the material that packages DNA within cells. Such changes can influence how easily genes are switched on or off.
“Interestingly, the way HSV-1 fine-tunes the immune response in microglia mirrors patterns seen in response to other factors associated with Alzheimer’s disease,” explains study co-author Kimberly Bruce, also from the University of Colorado Anschutz. “While we have not yet established that HSV-1 causes Alzheimer’s, this finding highlights the role of the microglial immune program as a common thread linking infection, aging, and genetic risk factors.”
“The development of Alzheimer’s disease is influenced by a multitude of genetic and environmental factors,” said Niemeyer. “Understanding how a common virus alters the immune environment of the brain may help us determine why some people become more vulnerable to neurodegenerative diseases.”
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