A new study from the University of Illinois Chicago reveals that herpes simplex virus-1 (HSV-1), commonly known for causing cold sores, can travel through the nasal cavity to the brain, leading to severe and lasting neurological symptoms. Researchers found that heparanase, a cellular enzyme, plays a critical role in allowing HSV-1 to cause damage to the brain.
In animal experiments, intranasal HSV-1 infection led to persistent neurological dysfunction, including anxiety and cognitive impairment. However, when the activity of heparanase was blocked, the severity of neurological damage was significantly reduced. This suggests that heparanase is a potential therapeutic target for mitigating the effects of neuroinflammation caused by viral infections.
The study’s findings highlight the need for prevention and treatment of HSV-1, which is estimated to be carried by nearly two-thirds of the global population. The virus can reactivate throughout life, making it essential to raise awareness among those carrying the virus.
According to the researchers, intranasal infection allows HSV-1 to bypass traditional entry points into the brain, potentially leading to more severe and long-lasting neurological symptoms. The study’s lead author, Deepak Shukla, emphasized the importance of addressing this aspect of HSV-1 infection, saying that “the neurological consequences are much more severe than you would normally see with fever blisters or ocular infection.”
The research is the first to show that a cellular enzyme can mediate behavioral symptoms in viral infections. The study’s findings position heparanase as a potential therapeutic target for preventing long-term brain injury caused by viral infections.
The researchers’ discovery has significant implications for the treatment and prevention of HSV-1-related neurological damage, highlighting the need for further research into this area.
Source: https://neurosciencenews.com/herpes-virus-neurology-28488