Is Parkinson’s linked to a virus we thought was harmless?
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We were surprised to find [this virus] in the brains of Parkinson’s patients at such high frequency and not in the controls. Even more unexpected was the way the immune system responded differently, depending on genetics.
Igor Koralnik, MD, Chief of Neuroinfectious Diseases and Global Neurology at Northwestern Medicine, press release
For years, the origins of Parkinson’s disease have puzzled neurologists. While genetics accounts for some cases, the majority of Parkinson’s remains idiopathic.
Now, a study from Northwestern Medicine published in JCI Insight is raising the possibility that a usually harmless virus might contribute to the disease.[]
More about the research
The research, led by Igor Koralnik, MD, Chief of Neuroinfectious Diseases and Global Neurology, investigated whether environmental factors—such as viruses—could be involved in Parkinson’s.
Using a sophisticated tool called ViroFind, the team scanned post-mortem brain tissue from individuals with Parkinson’s and controls, looking for any human-infecting viruses.
The result? Human Pegivirus (HPgV) was present in the brains of Parkinson’s patients, but not in those of controls.
HPgV, a blood-borne virus related to hepatitis C, is not known to cause disease. Yet, in patients with Parkinson’s, it appeared not only in the brain but also in cerebrospinal fluid.
“HPgV is a common, symptomless infection previously not known to frequently infect the brain,” Dr. Koralnik said. “We were surprised to find it in the brains of Parkinson’s patients at such high frequency and not in the controls. Even more unexpected was how the immune system responded differently, depending on genetics. This suggests [the virus] could interact with the body in ways we didn’t realize before.”
The study examined post-mortem brains from 10 people with Parkinson’s and 14 without. HPgV was found in the post-mortem brains of five of 10 people with Parkinson’s; it was not found in any of the 14 control brains.
Patients with the virus showed distinct neuropathological changes, including increased tau pathology and altered levels of specific brain proteins.
Blood analysis of samples from more than 1,000 participants in the Parkinson’s Progression Markers Initiative mirrored these findings. Immune signals differed between those with and without the virus, regardless of genetic background.
Yet, in patients carrying the Parkinson’s-linked LRRK2 mutation, immune responses to the virus were notably distinct from Parkinson’s patients without the mutation.
Next steps for the research team include expanding the cohort to determine how common the HPgV is in Parkinson’s patients and whether its presence contributes to disease development.
“One big question we still need to answer is how often the virus gets into the brains of people with or without Parkinson’s,” Dr. Koralnik noted. “We also aim to understanding how viruses and genes interact; insights that could reveal how Parkinson’s begins and could help guide future therapies.”
Related: Data shows more people are getting Parkinson’s younger—but why?What this means for you
Parkinson’s disease affects more than 1 million people in the United States, with 90,000 new cases annually. By 2030, that number is expected to rise to 1.2 million.
If HPgV or similar viruses play a role in disease progression, it could represent a new frontier in understanding, preventing, and ultimately treating Parkinson’s.
For neurologists, these findings are a reminder that environmental factors—including seemingly benign viruses—may interact with genetic risk in ways that have been largely unexplored.
It’s a call to watch this space: Future therapeutic strategies might one day involve targeting viral contributors, alongside traditional neuroprotective approaches.