Common blood virus detected in brains of Parkinson’s patients in Northwestern study

Researchers at Northwestern Medicine report finding remnants of a common blood-borne virus in the brains of people who had Parkinson’s disease, a discovery they say could point to a previously unrecognized contributor to the disorder.

In tissue analyses, investigators detected human pegivirus (HPgV) in about half of the brains from people with Parkinson’s and found no evidence of the virus in brains from individuals without the disease. Patients whose brains contained HPgV also displayed distinct immune responses and more advanced markers of brain damage than those without the virus.

The researchers said additional differences emerged when they examined blood samples. People with detectable HPgV in blood showed molecular signs indicating cells were struggling to produce energy and to remove damaged components, processes that are central to maintaining neuronal health. Genetic mutations known to influence Parkinson’s progression appeared to interact with the virus-associated changes, producing more pronounced brain abnormalities in some cases.

Parkinson’s disease gradually destroys dopamine-producing neurons in the brain, causing tremor, stiffness, balance problems and other movement disorders. The disease’s causes are incompletely understood, and scientists have long sought environmental and biological factors that might trigger or accelerate degeneration.

HPgV, a virus related to hepatitis C, is spread primarily through exposure to infected blood, such as through shared needles or blood transfusions before routine screening was implemented. The virus is not typically described as highly contagious through casual contact; many infections are asymptomatic and the pathogen has not previously been widely linked to neurodegenerative disease.

Researchers cautioned that the new findings describe an association and do not establish that HPgV causes Parkinson’s. The presence of viral remnants in brain tissue could reflect a variety of scenarios, including viral persistence after infection or secondary colonization of vulnerable tissue. Determining whether HPgV plays a causal role will require additional studies that replicate the result, define how and when brain infection occurs, and test mechanisms by which the virus might contribute to neuronal loss.

The Northwestern team said the work adds to a growing body of research investigating infectious and immune-related contributors to neurodegeneration. If subsequent research supports a causal link, the finding could prompt renewed examination of blood-borne exposure history in Parkinson’s patients and exploration of antiviral or immune-modulating strategies as possible prevention or treatment avenues. For now, the study underscores the need for further laboratory and epidemiological investigation to clarify the relationship between HPgV and Parkinson’s disease.