'Harmless' Virus Could Play a Role in Parkinson's Disease, New Findings Suggest

Recent research indicates that a common virus previously considered harmless to humans might be connected to the development of Parkinson's disease. The virus, known as Human Pegivirus (HPgV), was detected in half of the brain samples from individuals with Parkinson's, while it was absent in the brains of healthy individuals, according to the latest study published in JCI Insight.

Dr. Igor Koralnik, the lead researcher and chief of neuroinfectious diseases and global neurology at Northwestern Medicine in Chicago, emphasized that HPgV is typically an asymptomatic infection that rarely, if ever, infects the brain. The surprising discovery of its presence in Parkinson's patients' brains suggests a possible role in the disease's progression.

The study also found that HPgV influences immune responses differently depending on a person’s genetics. For example, individuals with a genetic mutation linked to Parkinson's, called LRRK2, exhibited distinct immune system signals, implying a complex interaction between the virus, genetics, and immune response.

Parkinson's disease manifests when dopamine-producing brain cells degrade or become impaired. This decline leads to motor symptoms such as tremors, stiffness, reduced coordination, and balance issues. In the U.S., over one million people live with Parkinson's, including notable figures like Michael J. Fox and Neil Diamond. The disease affects about 90,000 new cases annually.

To investigate further, researchers examined the brains of 10 Parkinson’s patients and 14 healthy controls. They found HPgV in five of the Parkinson’s brains but not in any of the healthy controls. Additionally, the virus was detected in the spinal fluid of Parkinson’s patients. Moreover, the Parkinson's group showed greater overall brain damage.

Further analysis of blood samples from more than 1,000 participants in the Parkinson's Progression Markers Initiative revealed that only around 1% of Parkinson’s patients carried HPgV in their blood. Interestingly, those infected exhibited different immune responses, especially among carriers of the LRRK2 mutation. This finding highlights the potential influence of viral infections and genetic factors in Parkinson’s development.

The researchers plan to study the frequency of HPgV in Parkinson’s patients and to explore how the virus might trigger neurodegeneration. A key question is how often HPgV enters the brain and interacts with genetic predispositions. Insights gained from future research could inform new therapeutic strategies and deepen our understanding of Parkinson’s disease origins.