Researchers have uncovered new clues that could help doctors understand why some people suffer from Parkinson’s disease.
A progressive neurological disorder affecting 10 million people globally, Parkinson’s can cause disruptive symptoms such as tremors, immobility and loss of balance.
Now, scientists at Northwestern Medicine have discovered that a usually harmless virus — the Human Pegivirus — may be a contributor to the disease.
The findings — published Wednesday in the journal JCI Insight — come shortly after Stanford researchers unveiled improved treatment, called adaptive Deep Brain Stimulation (aDBS) therapy, for the disease.
Northwestern researchers set out to find environmental factors that could trigger the condition by testing the brain matter of 10 people who had Parkinson’s when they died and 14 who did not.
“Using a tool called ViroFind, we analyzed post-mortem brain samples from individuals with Parkinson’s and from those who died of other causes. We searched for all known human-infecting viruses to identify any differences between the two groups,” Igor Koralnik, who led the study, said in a statement.
ViroFind is a time consuming and expensive but powerful process that draws upon a genomic library of over 565 viral species when analyzing substances in human cells. The tool also has the power to identify new viruses and viruses found only in animals for now but predicted to one day leap to humans.
The researchers found Human Pegivirus, or HPgV, in the brains and spinal fluid of people with Parkinson’s but not in those without the disease. The brains with HPgV also showed more advanced or distinct problematic changes, including altered levels of brain proteins such as tau proteins, which can lead to Alzheimer’s disease and frontotemporal dementia when they accumulate in neurons.
Blood-borne HPgV is in the same family as hepatitis C but has been considered a harmless, asymptomatic infection that does not cause disease and rarely enters the brain. According to Northwestern Medicine researchers, there is insufficient information about how HPgV is transmitted and contracted.
“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 a person’s genetics. This suggests it could be an environmental factor that interacts with the body in ways we didn’t realize before. 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,” Koralnik said.
The research also included blood analysis, made possible by samples from over 1,000 living participants of the growing Parkinson’s Progression Markers Initiative launched in 2010 by The Michael J. Fox Foundation and scientists to create a biosample library to aid and accelerate scientific research. The immune systems of people with HPgV in the brain showed changes in signaling patterns regardless of their genetic differences.
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But over time, the research revealed that the immune systems of Parkinson’s patients with a certain genetic mutation responded differently to HPgV than those of Parkinson’s patients without it.
Koralnik said future research will examine how genetic differences affect the body’s response to other viral infections to determine whether the responses are unique to HPgV or more broadly related to other viruses, as well. The research team also plans to study more people to see how often the HPgV virus enters the brains of Parkinson’s patients, whether it plays a causal role in the disease, and how viruses and genes interact.
The insights could reveal how Parkinson’s begins, guiding future therapies.