Viral risk factor found for Parkinson disease

Movement disorders

By Mardi Chapman

20 Jun 2019

The incidence of Parkinson disease is lower in patients with chronic hepatitis C (HCV) infection who received interferon-based antiviral therapy than in untreated HCV patients.

The findings, from a large Taiwanese study, support other epidemiological evidence for an association between HCV and risk of developing Parkinson disease.

It also offers the potential for lowering this risk in people with HCV.

From more than 188,000 people identified with HCV infection between 2003 and 2013, the study propensity matched 39,936 treated patients with 39,936 untreated patients.

The study determined the incidence density of Parkinson disease was 1.00 in the treated group and 1.39 in the untreated group.

Although the risk was not different at years 1 and 3, it was significantly different by year 5 (HR 0.75) and at the end of the cohort (HR 0.71).

The researchers said it was the first study to investigate the association between antiviral therapy and the risk of development of Parkinson disease (PD).

“The lower rate of PD occurrence in the treated patients may suggest that HCV infection is a risk factor for PD development, and antiviral therapy lowers the risk,” they said.

“It cannot be fully excluded that interferon-based antiviral therapy had a direct protective quality against the development of PD. However, the short exposure of antiviral agent, 16 to 48 weeks in most treated participants, makes protecting against PD development in 5 years less likely.”

They said neuroinflammation may help explain any link between HCV infection and the development of Parkinson disease.

“The underlying mechanism of the protective potential of interferon-based antiviral therapy could be complicated and may involve the modulation of antiinflammatory cytokines.”

“In contrast, the reduced incidence of PD by antiviral therapy could be associated with the reduction or clearance of HCV in patients.”

An accompanying editorial in JAMA Neurology said the findings add to the evolving knowledge about the association between immunological and infectious factors in PD and related disorders.

“Although pathogenic mechanisms between HCV infection and PD remain unconfirmed, it is possible that HCV infection enters the brain through the microvasculature and then induces microglial and macrophages inflammatory changes, with damage associated with the release of neurotoxins such as nitric oxide and proinflammatory cytokines, including tumor necrosis factor, IL-1, and IL-6.”

“Other potential mechanisms include immune cross-reactivity between HCV peptides and brain tissue antigens that leads to neurodegeneration.”

They said that while the search for disease-modifying or neurorestorative therapies for PD continues, identification of potentially treatable PD risk factors presents a unique opportunity for treatment.

“Additional studies with detailed viral analysis and exposure are needed, including in other geographic and ethnic distributions.”

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