Link Between Oral Herpes and Multiple Sclerosis Identified
Approximately half of all adults carry a virus that leads to cold sores and can cause blisters in the mouth.
Recent research from the University of Illinois Chicago (UIC) indicates that oral herpes, caused by the herpes simplex virus-1 (HSV-1), may also increase the risk of developing multiple sclerosis (MS), a condition that can significantly impact quality of life.
In their study, scientists gene-edited mice to prevent the creation of a protein known as optineurin, which is crucial for protecting the body against herpes infections, before infecting them with the virus.
This infection resulted in rapid deterioration of the myelin sheath, a protective layer surrounding nerve fibers. The mice exhibited symptoms similar to MS, including muscle weakness and coordination difficulties.
This aligns with observations in MS patients, where the immune system incorrectly attacks the myelin sheath.
The researchers suggest that their findings could outline a potential connection between HSV-1 and MS, distinguishing it from the HSV-2 virus that leads to genital herpes.
Dr. Deepak Shukla, a molecular virology professor at UIC and the study’s lead, mentioned, “Our findings deepen our understanding of viral development and open up possible ways to reduce viral-induced nerve damage.”
He added that an ongoing battle between the virus and the immune system could lead to damage if a person becomes immunocompromised.
Oral herpes is widespread, affecting about 47% of adults, or roughly 124 million individuals, according to CDC data.
This virus primarily spreads through sexual contact, including kissing and oral sex, and while there’s no cure, it typically remains dormant, causing occasional outbreaks of sores.
Optineurin serves to manage the infection by limiting its spread and protecting against myelin sheath damage.
Earlier research has identified that being infected with Epstein-Barr virus (EBV) significantly raises the risk of MS, with about 95% of adults having experienced EBV, and estimates suggest it boosts MS risk by roughly 30%.
Other herpes viruses, such as those leading to chickenpox, shingles, and human herpes virus 6, are also connected to the onset or worsening of MS, which impacts about one million people in the United States.
MS is a debilitating autoimmune disorder that affects the brain and spinal cord, resulting in mobility issues, memory challenges, and fatigue.
In prior studies, Dr. Shukla’s team discovered that HSV-1 prompted a significant immune response in the brains of mice, leading to issues with memory, coordination, and anxiety.
They also found that optineurin helps combat the virus by decelerating its growth and dissemination.
In this latest examination, researchers infected mice without optineurin with the oral herpes virus in their eyes.
The results revealed that these mice experienced higher infection rates after four days, consistent with previous tests.
The researchers also observed that a protein called MLKL (Mixed Lineage Kinase Domain-Like protein) – produced during cell death – increased HSV-1 infections in the absence of optineurin.
This protein assisted the virus in entering a cell’s nucleus, hastening the infection, while optineurin curbed HSV-1 by instigating the breakdown of MLKL.
Imaging revealed significant aggregation of MLKL in the brains of these mice following HSV-1 infection, a phenomenon not observed in control mice.
These protein clumps seemed to lead to the death of oligodendrocytes, which are essential for producing the myelin sheath around neurons.
The absence of this sheath leaves the nervous system susceptible to damage.
The resultant harm disrupts communication between the brain and body, causing various symptoms associated with MS, including weakness, fatigue, coordination problems, and cognitive changes.
Identifying this protein could pave the way for new MS treatments. Shukla’s lab has already shown that necrosulfonamide, which inhibits optineurin, can help maintain nerve function in animal models.
Such studies bring hope for improving MS outcomes and may lead to earlier interventions or even potential cures.





