Herpes Infects Our Brains More Easily Than We Thought, Mouse Study Suggests

The herpes simplex virus (HSV) could be sneaking into the brain more often than we’re aware.

A new study on mice has found that when HSV type 1 infection accesses the body through the nose, it can lead to rapid nerve damage and high levels of inflammation in the mammal brain.

The consequences may be far worse than oral or genital sores. Several months after viral exposure, researchers measured increased anxiety, motor impairment, and cognitive issues in mice.

“There is definitely nerve damage if you take the intranasal route, and the effects are long-term, which is alarming,” says ophthalmologist Deepak Shukla from the University of Illinois Chicago (UIC).

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It is unclear if the same dire consequences occur in humans, who are more used to herpes infections as a species and have developed natural defenses. That said, in rare clinical cases, the herpes virus is known to infect the human eye, nose, and brain, potentially causing severe and permanent neurological consequences.

Researchers at UIC think the nasal route could be an overlooked way the virus is sneaking into our central nervous systems, bypassing the blood-brain barrier which usually keeps viruses out.

“If an infected individual is shedding virus via tears, it could reach the nasal cavity, where it could go more directly to the brain,” suggests Shukla.

“I think it’s underdiagnosed and understudied, but the neurological consequences, we believe, are much more severe than you would normally see with fever blisters or ocular infection.”

In patients with HSV-1 infections in their eyes, scientists have noticed elevated levels of an enzyme called heparanase (HPSE). HPSE is triggered by the presence of HSV-1, and this protein seems to contribute to an inflammatory response.

When mouse brains are infected with HSV-1 via the nose, researchers at the University of Illinois Chicago found HPSE had a similar, inflammatory role to play in the brain.

Compared to regular mice, those that had the gene that creates HPSE deleted showed less neuroinflammation and better cognitive outcomes after nasal infection with the herpes virus.

Mice with the natural ability to create HPSE, meanwhile, showed rapid disease progression, with poorer memory, higher anxiety, and lower motor coordination overall.

“These findings suggest that targeting HPSE could be a promising therapeutic strategy for reducing HSV-1-induced neuroinflammation and preserving cognitive and motor function,” the authors write.

And that may prove beneficial for more than just a rare few. While severe infections of HSV-1 in the human central nervous system are uncommon, the ability for herpes to infiltrate the brain and persist in the central nervous system for years on end may not be.

In 2008, researchers discovered the DNA of HSV-1 in 90 percent of all the protein plaques they looked at in postmortem brains of Alzheimer’s patients.

More recently, a long-term study found those exposed to the herpes simplex virus type 1 face double the risk of developing dementia.

There is no cure for the herpes simplex virus, which can reactivate throughout life. Figuring out why and how this happens could help limit its potentially long-term degenerative effects.

For instance, human mini-brain models have recently revealed that physical trauma can reawaken dormant herpes infections in the nervous system, possibly leading to inflammation and protein clumps and tangles associated with degenerative diseases, like Alzheimer’s.

The recent findings on pro-inflammatory markers like HPSE suggest that one of the most common viral infections in the world – impacting as much as two-thirds of the global population – may be a neglected source of cognitive decline.

“These insights open the door to potential therapeutic approaches to mitigate the effects of neuroinflammation and prevent long-term brain injury caused by viral infections,” says Hemant Borase, a UIC biochemist and first author of the study.

The study was published in mBio.