Scientists discovered strikingly high levels of a common virus in the brains of people with Parkinson’s disease, a finding that points to a potential cause for the neurological disorder.
Researchers from Northwestern Medicine analyzed the brains of people who had Parkinson’s and some of those without it. They found remnants of the human pegivirus (HPgV) in half of all brains with Parkinson’s and none in the brains of those without.
Patients with the virus had distinct immune responses and advanced brain changes, which were further impacted by genetic mutations. Parkinson’s gets worse over time, gradually degrading the part of the brain that produces dopamine, a chemical critical for controlling movement, which causes tremors, stiffness and falls.
People with Parkinson’s who had the virus in their brains showed more advanced brain damage. Those who had the virus in their blood also showed signs that their cells were struggling to produce energy and clean out damaged parts.
HPgV is spread through blood and is a close relative of the Hepatitis C virus. However, unlike Hepatitis C, HPgV was not previously believed to cause any illness and was thought to lie dormant in the body. This latest study challenges that assumption, suggesting it may play a role in Parkinson’s disease.
Dr Igor Koralnik, chief of neuroinfectious diseases and global neurology at Northwestern Medicine, said in a statement: ‘For a virus that was thought to be harmless, these findings suggest it may have important effects, in the context of Parkinson’s disease. It may influence how Parkinson’s develops, especially in people with certain genetic backgrounds.’
The exact cause of Parkinson’s – which affects about one million Americans causing trouble walking and cognitive problems – is still unknown. Researchers have been studying possible contributors for years, and viruses are among several possibilities.
When the brain detects a virus, it triggers inflammation as a defense mechanism. While this is meant to fight the infection, chronic or overzealous inflammation can accidentally damage or kill delicate brain cells, including the dopamine-producing neurons.
Michael J Fox, pictured in April 2025, is one of the most high-profile Parkinson’s sufferers. He founded The Michael J Fox Foundation for Parkinson’s Research, which has been responsible for landmark research into the disease
For the blood analysis, researchers turned to a library of samples from over 1,000 participants in the Parkinson's Progression Markers Initiative (PPMI), a major study launched by The Michael J Fox Foundation to accelerate research and treatment discovery.
Scientists analyzed the brain tissue of 24 deceased individuals. Ten of them had Parkinson's when they died, and 14 did not. They detected the virus in half of the Parkinson's brains and in none of the brains from the control group.
HPgV is a common, symptomless infection previously not known to infect the brain. As of 2024, studies estimate that about four percent of Americans have an active HPgV infection, and up to 12 percent have been exposed to the virus at some point in their lives
The primary route of transmission is through exposure to infected blood, such as from shared needles or, historically, through blood transfusions before widespread screening.
In patients with a specific Parkinson’s-related gene mutation, LRRK2, the body’s immune system reacted more aggressively to the virus compared to Parkinson’s patients without the mutation.
The gene mutation rewired the brain's immune circuitry when the virus was present in the blood, leading to a dysfunctional and harmful inflammatory response that would not have happened if the person had either the virus or the gene mutation alone, but not both together.
The ensuing inflammation in the brain led to brain damage that contributed to Parkinson's. It damages and kills neurons, particularly the dopamine-producing cells in the brain region known as the substantia nigra, a hallmark of Parkinson's disease.
‘We were surprised to find it in the brains of Parkinson’s patients at such high frequency and not in the controls,’ Dr Koralnik said. ‘Even more unexpected was how the immune system responded differently, depending on a person’s genetics.
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‘This suggests it could be an environmental factor that interacts with the body in ways we didn’t realize before.’
Researchers also detected the virus in the spinal fluid of Parkinson's patients, but not in those without the neurological disorder.
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In Parkinson’s disease, the area of the brain that produces dopamine begins to deteriorate.
In addition to playing a crucial role in the brain’s reward system, dopamine is key to the brain's movement control system.
Without sufficient dopamine, the brain's movement circuit becomes impaired, leading to stiffness and tremors, as well as difficulty initiating movement, such as getting up from a chair, and slowness.
Patients with the virus in their brain tissue also had a greater build-up of toxic tau protein and abnormal levels of key brain proteins, indicating very advanced disease.
Tau is a protein that typically helps stabilize microtubules, the internal scaffolding of brain cells.
When it becomes damaged and misfolded, it is a general sign that the brain cell is failing.
Dopamine levels in the brain from normal levels to Parkinson’s affected levels (left to right)
Finding more tau pathology in these patients is a strong indicator that the virus is associated with more widespread brain cell damage and dysfunction, not just the specific dopamine cell loss typical of pure Parkinson's.
The results were published in the journal JCI Insight.
Treatment options for Parkinson’s are limited in what they accomplish. They mainly provide symptomatic relief by managing motor symptoms, but they cannot cure or slow the progression of the disease.
Levodopa (L-Dopa) is the gold standard and most effective treatment. The brain converts L-Dopa into dopamine, which directly replaces the missing chemical that is causing the core movement symptoms.
More than 10 million people worldwide, including about 1million Americans, are estimated to have Parkinson’s disease, and that number is to grow to more than 25 million by 2050.
Dr Koralnik said: ‘We plan to look more closely at how genes like LRRK2 affect the body’s response to other viral infections to figure out if this is a special effect of HPgV or a broader response to viruses.
‘One big question we still need to answer is how often the virus gets into the brains of people with or without Parkinson’s. We also aim to understand how viruses and genes interact; insights that could reveal how Parkinson’s begins and could help guide future therapies.’