Common ‘harmless’ virus detected in brains and spinal fluid of Parkinson’s patients, study finds
Northwestern Medicine researchers found Human Pegivirus in post-mortem brain tissue and spinal fluid of people with Parkinson’s but not in matched controls; authors urge larger studies before drawing causal conclusions.
Researchers at Northwestern Medicine report detecting Human Pegivirus (HPgV) in the brains and spinal fluid of people with Parkinson’s disease, a finding the team says challenges assumptions that the virus is symptomless and rarely infects the nervous system.
The study, published in JCI Insight, examined post-mortem brain tissue from 10 people who had Parkinson’s and 14 who died of other causes. HPgV was detected in brain tissue from five of the 10 Parkinson’s cases and in none of the 14 controls. The virus also appeared in cerebrospinal fluid samples from patients with Parkinson’s, suggesting it may be present and active in the nervous system.
Investigators said additional laboratory and blood-sample analyses reinforced the initial tissue findings. Using blood specimens from more than 1,000 participants in a project led by The Michael J. Fox Foundation, the team identified immune-system changes consistent with HPgV exposure. The Northwestern group also reported that patients who carried HPgV tended to show more advanced brain changes associated with Parkinson’s, including protein buildup and altered brain chemistry.
The researchers further noted an interaction between the virus and a known genetic risk factor: people with a Parkinson’s-related mutation in the LRRK2 gene appeared to respond differently to HPgV than those without the mutation. "HPgV is a common, symptomless infection previously not known to frequently infect the brain," said Dr. Igor Koralnik, chief of neuroinfectious diseases at Northwestern. "We were surprised to find it in the brains of Parkinson’s patients at such high frequency and not in the controls."
Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s, and most cases do not have a clear inherited cause. About 90,000 Americans are diagnosed each year, and estimates from the Parkinson’s Foundation project the number of people living with the disease in the United States could reach 1.2 million by 2030. Researchers say identifying environmental or infectious contributors could help explain why some people develop Parkinson’s while others do not.
Independent experts cautioned against interpreting the new results as proof that HPgV causes Parkinson’s. "The study detected traces of HPgV more often in brains of people with Parkinson’s disease than in controls. This raises the possibility of a link between viral exposure and Parkinson’s, but it’s far too early to say the virus causes the disease," said Dr. Joel Salinas, a behavioral neurologist and associate professor at NYU Grossman School of Medicine, who was not involved in the research. He said larger and longer-term studies will be required to determine clinical significance.
The Northwestern team acknowledged limitations in the current work. The post-mortem tissue analysis involved a small number of brains, and the researchers said they plan to expand their sample size and look for HPgV in a broader set of people with Parkinson’s and in healthy controls. They also intend to investigate whether other viruses may be involved and to further characterize how viral exposure and specific genetic backgrounds, such as LRRK2 mutations, might interact.
If future research confirms a role for HPgV or other infectious agents in Parkinson’s development, it could open new avenues for prevention or treatment focused on antiviral strategies or modulation of immune responses. Until then, researchers and clinicians urge caution and emphasize that this study represents an early step in exploring a potential infectious link to a complex neurodegenerative disease.
The authors said their next steps will include larger epidemiological and mechanistic studies to determine how often HPgV is found in people with Parkinson’s compared with healthy controls, whether HPgV persists or replicates in nervous tissue, and how viral presence might relate to disease progression.
The study’s publication adds to a broader scientific conversation about possible infectious or immune contributors to neurodegenerative disorders, a line of inquiry that has been pursued in other conditions such as Alzheimer’s disease but has not yet yielded definitive causal relationships.