About one in two adults is infected with a virus that can cause cold sores, fever and blisters in the mouth.

However, researchers at the University of Illinois Chicago (UIC) now propose that oral herpes, prompted by the herpes simplex virus-1 (HSV-1), might also increase the risk of developing multiple sclerosis, a life-altering condition.

In a recent study, scientists used gene editing on mice to prevent them from producing a protein known as optineurin, which is vital in defending against herpes infections, and subsequently infected these mice with the virus.

This infection resulted in the swift degradation of the myelin sheath, a protective layer on nerve fibers, causing the mice to exhibit MS-like symptoms, including muscle weakness, loss of movement, and impaired muscle coordination.

This mirrors the process observed in individuals with multiple sclerosis, where the myelin sheath also degrades because the immune system misfires and starts to attack the area.

The scientists say their findings could indicate a link between HSV-1, which is different from the HSV-2 virus that causes genital herpes, and MS.

Dr Deepak Shukla, a professor of molecular virology at UIC and the study’s lead, said: ‘Our findings enhance our understanding of how viruses develop and offer potential avenues for mitigating viral-induced [nerve cell] damage.

‘If you are infected, then your immune system is constantly locked in battle with the virus. And if for any reason you become immunocompromised, the virus can escape and damage your brain.’

Researchers have warned over a potential connection between oral herpes and multiple sclerosis (stock image, there is no suggestion that the above patient has herpes)

Oral herpes is an extremely common condition that infects about 47 percent of adults, according to the CDC, or 124million people.

The virus is spread via sexual contact, such as kissing and oral sex, and is incurable, normally lying dormant and triggering occasional flare-ups of sores on and around the mouth and lips.

In cells, it is controlled by the protein optineurin, which stops an infection from spreading and protects against any potential myelin sheath damage.

Scientists have previously established that one of the biggest risk factors for MS is an infection with the Epstein-Barr virus (EBV), a virus that has infected 95 percent of adults and which is estimated to raise the risk of MS by 30 percent.

And other herpes viruses, like the ones that cause chickenpox, shingles, and human herpes virus 6, have also been linked to the onset and worsening of MS, which affects 1 million Americans.

And MS is a debilitating, incurable autoimmune condition that affects the brain and spinal cord and leaves people with mobility issues, memory loss and fatigue. 

In earlier studies, Dr Shukla’s team found that HSV-1 triggered a strong immune response in the brains of mice, causing memory problems, poor coordination, and anxiety.

They also discovered that the protein optineurin helps fight the virus by slowing its growth and spread.

In the latest study, researchers infected mice that could not produce the protein with the oral herpes virus in their eyes.

Researchers only tested herpes simplex virus-1, or the virus that causes oral herpes. This differs from the one that causes genital herpes

As seen in earlier cell tests, mice without optineurin had higher infection rates after four days.

The researchers also found that a protein called MLKL, or Mixed Lineage Kinase Domain-Like protein, which is made by the body during cell death, boosted HSV-1 infections in the absence of optineurin.

Researchers said the protein facilitated the transportation of the virus into a cell’s nucleus, speeding an infection, and optineurin controlled HSV-1 infection by triggering the deterioration of MLKL.

Imaging studies revealed extensive clumping, or aggregation, of MLKL in the brains of optineurin-lacking mice, but not in control mice, in response to HSV-1 infection.

Also, these clumps appeared to trigger the death of myelin-producing oligodendrocytes, or cells that create armor, or the myelin sheath, around neurons.

Without the sheath, the nervous system was left vulnerable to damage.

The resulting damage disrupts the communication between the brain and the rest of the body, leading to the various symptoms associated with MS, such as weakness in the legs, fatigue, coordination problems, cognitive changes, and pain.

Identifying this protein offers a new target for multiple sclerosis therapies. Already, Shukla’s lab has demonstrated that necrosulfonamide, which inhibits optineurin, can preserve nerve function in animal models.

Studies like these provide hope for the future of MS, and bring about the potential to enable earlier intervention or a possible cure.