HCV infection raises risk of developing Parkinson’s

February 12, 2016

A new study indicates that infection with the hepatitis C virus (HCV) significantly increases the risk of developing Parkinson’s Disease.

Infection with the hepatitis C virus (HCV) significantly increases the risk of developing Parkinson Disease, according to a large epidemiologic study.

“We found an elevated risk of Parkinson’s Disease in patients infected with HCV. This does not mean HCV infection should become a mandatory test in Parkinson’s Disease patients. However, for those with HCV infection, clinicians should probably notice if there is any Parkinsonian features, such as bradykinesia, rigidity, or posture instability,” lead author, Hsin-Hsi Tsai, MD,  of the neurology department atNational Taiwan University Hospital, told Medical Economics.

Tsai and colleagues published the results online on December 23, 2015, in Neurology.

Using large samples in a nationwide population-based cohort, the researchers confirmed the association between HCV infection and Parkinson’s Disease. This association was not observed in hepatitis B virus (HBV) infection.

The analysis included 49,967 patients with viral hepatitis-35,619 (71.3%) with HBV infection, 10,286 (20.6%) with HCV infection, and 4062 (8.1%) with both infections. The patients, mean age 46, were followed for 12 years. They were compared to nearly 200,000 people without viral hepatitis.

“Our study discovered a 2.5-fold increased risk of Parkinson’s Disease in patients with HCV infection than controls (no HCV or HBV). After adjustment for age, sex, and multiple comorbidities, there was still a 1.3-fold increased risk,” said Tsai.

 

The study is limited by no information about the patients’ transfusion history and drug abuse, which are HCV risk factors.

The connection may be due to HCV entering the central nervous system (CNS) by disrupting the integrity of the blood-brain barrier, she said. “There is evidence that the essential HCV receptors are expressed on brain microvascular endothelial cells, a major component of the blood-brain barrier, compromising its integrity, and allowing entry into the CNS,” Tsai said.

This link is further supported by findings that HCV infection might release inflammatory cytokines, which may play a role in the pathogenesis of Parkinson’s Disease. “Viruses may directly injure neurons by viral replication or through activation of both innate and adaptive immune responses, resulting in neuronal damage through inflammation,” Tsai said.

Other viruses have also been associated with Parkinson’s Disease. “One of the most famous examples is the Parkinsonism that occurred subsequent to a viral encephalopathy that developed following the 1918 influenza pandemic caused by a type A H1N1 influenza virus. People born during the time of the pandemic outbreak of 1918 of influenza have a 2-3 fold increased risk of Parkinson’s Disease than those born prior to 1888 or after 1924,” Tsai said.

Another example is the human immunodeficiency virus (HIV). HIV can cause CNS involvement, leading to motor dysfunction, such as bradykinesia, cogwheel rigidity, and tremor. A number of other viruses, including Coxsackie, Japanese encephalitis B, western equine encephalitis, and herpes have also been linked to Parkinsonism. The mechanism has not been defined, but may be related the ability to enter the CNS, she said.

 

Tsai added that more research is needed to determine whether subclinical Parkinsonism is more prevalent in patients with HCV infection than in normal controls.