STUDY FINDS
Many people don’t know just how common the virus that causes cold sores is in society. Unfortunately, the news just got worse for those carrying Herpes Simplex Virus type 1. Researchers at the University of Colorado Anschutz Medical Campus have found that HSV-1 can make its way into the brain and potentially contribute to neurological diseases.
The study, published in the Journal of Virology, reveals that HSV-1 has the ability to spread into the central nervous system and target specific regions of the brain, including areas that control vital functions like sleep, movement, mood, and hormonal regulation.
“Recently, this common virus has been implicated in neurodegenerative diseases, such as Alzheimer’s disease, but no clear route of central nervous system invasion has been established,” explains Christy Niemeyer, PhD, an assistant professor of neurology at CU Anschutz and corresponding author of the study, in a media release.
The researchers set out to map the specific brain regions that HSV-1 infects and determine whether the virus migrates randomly or targets certain areas. They found that the virus preferentially infects critical regions like the brain stem, which controls sleep and movement, as well as areas that produce key neurotransmitters like serotonin and norepinephrine.
Notably, the team also observed that even after the virus was no longer detectable, the brain’s immune cells, called microglia, remained in an “inflamed” state in some regions. This persistent inflammation can potentially lead to chronic problems and may contribute to the development of neurological and neurodegenerative diseases.
“Identifying the role of microglia provides helpful clues to the consequences of HSV-1 infection, and how it triggers neurological diseases,” Niemeyer says. “Persistently inflamed cells can lead to chronic inflammation, a known trigger for a number of neurological and neurodegenerative diseases. This research offers important takeaways in better understanding how viruses interact with overall brain health as well as the onset of pervasive neurological diseases.”
The study, which examined the brains of mice infected with HSV-1, offers a crucial first step in understanding how this common virus can infiltrate and potentially impact the human brain. Estimates show that anywhere between 50% and 80% of American adults carry HSV-1, even if they don’t display symptoms.
“Identifying how HSV-1 can get into the brain and what brain regions are vulnerable is key in understanding how it initiates disease,” Niemeyer concludes.
This newfound knowledge could pave the way for further research into the links between HSV-1 and neurological disorders, potentially leading to improved prevention, early detection, and targeted treatment strategies in the future.
The researchers used adult C57BL/6 mice to understand how HSV-1 spreads from the nasal passages to the brain. To model infection, they injected HSV-1 into the noses of anesthetized mice, with some mice receiving only a mock injection as a control. After infection, they tracked the virus spread in the nasal and brain regions over several time points (from 7 hours to 10 days post-infection).
Tissue samples from the nose and brain were preserved, sectioned, and stained to identify virus-infected areas and the activation state of microglia, the brain’s immune cells. Observing these tissues under specialized microscopes allowed them to visualize the spread of HSV-1 and how microglial cells responded to infection.
The study found that HSV-1 initially infected the nose, especially the olfactory epithelium (the smell-sensing tissue) and respiratory tissue. The virus spreads from these areas to specific brain regions, especially those connected by the trigeminal and vagus nerves, like parts of the brainstem and hypothalamus.
