Mouse Study Suggests Herpes Can Infect the Brain More Easily Than Expected

A recent study ^[1], published in the journal mBio, on mice revealed that the herpes simplex virus (HSV) could enter the body via the nose and can rapidly damage the nerves and cause brain inflammation.

The repercussions may be more severe than genital or oral sores. Many months later after exposure to the herpes virus, the researchers found that mice seemed to have increased anxiety, motor, and cognitive issues.

Dr. Deepak Shukla, an ophthalmologist from the University of Illinois Chicago, stated that there is definite nerve damage via the intranasal route and the effects are long-term, which is concerning.

It is uncertain if humans experience the same consequences since we have developed natural defenses against herpes infections over time. There are rare instances where the herpes virus is known to infect the nose, brain, and eyes, which have resulted in consequences like severe and permanent neurological damage.

The researchers think the way the herpes virus enters through the nasal route is often overlooked. It can bypass the blood-brain barrier, which is supposed to prevent the entry of the virus.

Dr. Shukla thinks it is not well researched and diagnosed and that the neurological consequences are likely more severe than typical fever blisters or ocular infection. He also added that if an infected individual sheds the herpes virus through tears, it may reach the nasal cavity and lead to the brain.

The researchers noticed that an enzyme called heparanase (HSPE) is elevated in patients with HSV-1 eye infections. HSPE gets activated in the presence of HSV-1, thereby contributing to an inflammatory response.

A similar inflammatory response in the brain was noted by the researchers when the mouse brains were infected with HSV-1. The mice without the gene that creates HSPE had less neuroinflammation and better cognitive outcomes than regular mice. Whereas, the mice that could naturally produce HSPE showed faster disease progression as well as poor memory, increased anxiety, and overall poor motor coordination.

The authors wrote that the findings from this study show that targeting HSPE could be a hopeful treatment strategy to reduce HSV-1-induced neuroinflammation as well as protect motor and cognitive function. It may potentially be helpful for a larger group of people too.

Even though severe HSV-1 infections in the central nervous system (CNS) are rare, it is not possible that the virus can infiltrate the brain and remain in the CNS for a long time. In 2008, DNA of HSV-1 was discovered in 90% of all the protein plaques studied in brains of Alzheimer’s patients.

Recently, a study ^[2] revealed that people exposed to HSV-1 are twice as likely to develop dementia. There is no remedy for the herpes virus, as it can reactivate at any point in life. Finding out the exact cause could reduce the possible long-term degenerative effects.

For example, physical trauma is a possible cause for reactivation of a dormant herpes infection in the nervous system, which in turn leads to inflammation and clumping of proteins in diseases like Alzheimer’s.

Dr. Hemant Borase, a biochemist at the University of Illinois Chicago and the first author of the study, stated that the study findings pave the way for possible treatment strategies that can reduce the effects of neuroinflammation and also prevent the long-term brain injury caused by viral infections.

References:

1. "HPSE-Mediated Proinflammatory Signaling Contributes to Neurobehavioral Deficits Following Intranasal HSV-1 Infection." mBio. Accessed March 12, 2025. https://journals.asm.org/doi/10.1128/mbio.03765-24.

2. "Herpes Simplex Viral Infection Doubles the Risk of Dementia in a Contemporary Cohort of Older Adults: A Prospective Study." Journal of Alzheimer's Disease. Accessed March 12, 2025. https://content.iospress.com/download/journal-of-alzheimers-disease/jad230718?id=journal-of-alzheimers-disease%2Fjad230718.

(Input from various sources)

(Rehash/Dr. Nethra Suryanarayanan/MSM)