Herpes simplex virus type 1 (HSV-1), which causes the common cold, has long been known to affect the brain and central nervous system.
Researchers at the University of Colorado and the University of Bourgogne in France recently studied a search This provides new information about how the virus spreads inside the brain.
The researchers mapped the areas affected by the virus using mouse models to study how HSV-1 affects different parts of the brain. Their findings suggest that HSV-1 can reach the central nervous system through two main pathways: the trigeminal nerve, which connects the face and the brain, and the olfactory nerve, which is responsible for the sense of smell. Despite identifying these entry points, the exact mechanism of how HSV-1 spreads within the brain remains unclear.
“Recently, this common virus has been implicated in neurodegenerative diseases such as Alzheimer’s disease, but no clear route of invasion of the central nervous system has been established,” said Christy Neimeyer, MD, assistant professor of neurology at the University of Colorado Anschutz Medical Campus. , says Ph.D. and co-first and corresponding authors. “Identifying how HSV-1 can enter the brain and which areas of the brain are vulnerable is important in understanding how it initiates the disease.”
Once HSV-1 enters the brain, the researchers also wanted to determine whether the virus moved randomly or to specific areas. They were able to trace where and how the virus traveled within the brain and infected critical brain areas that control many vital functions, such as the brain stem, which controls sleep and movement. Researchers also found HSV-1 in areas of the brain that produce serotonin and norepinephrine, as well as the hypothalamus, an important center of appetite, sleep, mood and hormonal control within the brain.
“Even if the presence of HSV-1 is not causing full-blown encephalitis in the brain, it can still affect the way these areas function,” Niemeyer says.
Niemeyer and coauthors also show how HSV-1 interacts with key immune cells in the brain; Microglia. They found that microglia became “inflamed” when interacting with HSV-1, but in some areas of the brain, the inflamed microglia persisted even after the virus was no longer detected.
“Identifying the role of microglia provides helpful clues about the consequences of HSV-1 infection and how it triggers neurological diseases,” says Niemeyer. “Persistent inflammatory cells can lead to chronic inflammation, a known trigger for many neurological and neurodegenerative diseases. This research provides important suggestions into better understanding how viruses affect overall brain health as well as the onset of broader neurological diseases.” How to get in touch with.”
This study increases the understanding of the impact of HSV-1 on the brain, which is an important step toward developing treatments to limit its impact on the nervous system.
