Summary: Research has shown that HSV-1, the virus responsible for cold sores, can spread into specific areas of the brain and may contribute to neurodegenerative diseases. Mapping HSV-1’s path reveals it targets regions crucial for functions like sleep, movement, and mood regulation.
The study also found that HSV-1 activates the brain’s immune cells, causing inflammation that could persist even after the virus clears. This prolonged inflammation may be a trigger for neurological diseases.
Understanding HSV-1’s interactions in the brain could inform future treatments. The findings offer vital clues on how this common virus may play a role in the onset of diseases like Alzheimer’s.
Key Facts:
- HSV-1 targets brain areas like the hypothalamus, impacting mood and hormonal control.
- HSV-1 activates microglia, the brain’s immune cells, causing persistent inflammation.
- Chronic inflammation from HSV-1 may lead to neurological and neurodegenerative diseases.
Source: University of Colorado
Herpes simplex virus type 1 (HSV-1), the cause of the common cold sore, can spread into the central nervous system and preferences for certain parts of the brain.
Study results published today in the Journal of Virology are among the first to recognize how this common virus infiltrates the brain, leading to a better understanding of how HSV-1 may trigger neurological diseases.
“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,” says Christy Niemeyer, PhD, assistant professor of neurology at the University of Colorado Anschutz Medical Campus and co-first and corresponding author.
“Identifying how HSV-1 can get into the brain and what brain regions are vulnerable is key in understanding how it initiates disease.”
Once HSV-1 enters the brain, researchers also wanted to determine if the virus migrates at random or to specific areas. They were able to map where and how the virus travels within the brain and infects critical brain regions that control many vital functions, such as the brain stem, which controls sleep and movement.
Researchers also found HSV-1 in regions of the brain that produce serotonin and norepinephrine, as well as the hypothalamus, a critical center of appetite, sleep, mood, and hormonal control within the brain.
“Even though the presence of HSV-1 is not causing full-blown encephalitis in the brain, it can still affect how these regions function,” says Niemeyer.
Niemeyer and coauthors also show how HSV-1 interacts with the brain’s key immune cells; microglia. They found that microglia became “inflamed” when interacting with HSV-1, but in some brain regions, inflamed microglia persisted even after the virus was no longer detected.
“Identifying the role of microglia provides helpful clues to the consequences of HSV-1 infection, and how it triggers neurological diseases,” says Niemeyer.
“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.”
About this neurology research news
Author: Kelsea Pieters
Source: University of Colorado
Contact: Kelsea Pieters – University of Colorado
Image: The image is credited to Neuroscience News
Original Research: Closed access.
“Olfactory and trigeminal routes of HSV-1 CNS infection with regional microglial heterogeneity” by Christy Niemeyer et al. Journal of Virology
Abstract
Olfactory and trigeminal routes of HSV-1 CNS infection with regional microglial heterogeneity
Herpes simplex virus type 1 (HSV-1) primarily targets the oral and nasal epithelia before establishing latency in the trigeminal ganglion (TG) and other peripheral ganglia.
HSV-1 can also infect and become latent in the central nervous system (CNS) independent of latency in the TGs.
Recent studies suggest entry to the CNS via two distinct routes: the TG-brainstem connection and olfactory nerve; however, to date, there is no characterization of brain regions targeted during HSV-1 primary infection.
Furthermore, the immune response by microglia may also contribute to the heterogeneity between different brain regions. However, the response to HSV-1 by microglia has not been characterized in a region-specific manner.
This study investigated the time course of HSV-1 spread within the olfactory epithelium (OE) and CNS following intranasal inoculation and the corresponding macrophage/microglial response in a C57BL/6 mouse model.
We found an apical to basal spread of HSV-1 within the OE and underlying tissue accompanied by an inflammatory response of macrophages. OE infection was followed by infection of a small subset of brain regions targeted by the TG in the brainstem and other cranial nerve nuclei, including the vagus and hypoglossal nerve.
Furthermore, other brain regions were positive for HSV-1 antigens, such as the locus coeruleus (LC), raphe nucleus (RaN), and hypothalamus while sparing the hippocampus and cortex.
Within each brain region, microglia activation also varied widely. These findings provide critical insights into the region-specific dissemination of HSV-1 within the CNS, elucidating potential mechanisms linking viral infection to neurological and neurodegenerative diseases.
