Hepatitis C May Increase Risk Of Parkinson's

Hepatitis C virus may damage dopamine neurons in the brain. Ralwel/Shutterstock

It’s in the name: Hepatitis C virus (HCV) is the causative agent of hepatitis C, an infectious disease of the liver. So it will probably come as quite a surprise that this agent has now been linked with one of the most common neurodegenerative diseases, Parkinson’s.

Described in the journal Neurology, scientists from China Medical University examined data from close to 250,000 individuals that was obtained from the National Health Insurance Database of Taiwan. Of these participants, 49,967 had hepatitis, while 199,868 did not. Those in the former group were categorized according to disease etiology: individuals with hepatitis B virus (71 percent), hepatitis C virus (21 percent), or both (8 percent).

These participants were then followed for an average of 12 years, in which any diagnoses of Parkinson’s were recorded. In total, 1,330 individuals developed the disease throughout the course of the study, 270 of which also had hepatitis.

Although less than half of the latter group had hepatitis C, after taking into account potentially confounding factors like age, sex, and the presence of severe liver scarring (cirrhosis), the researchers found that hepatitis C was linked with a 30 percent greater risk of developing Parkinson’s when compared with those without hepatitis. The same relationship was not observed for hepatitis B, though, which was associated with neither an increased nor diseased risk of developing Parkinson’s.

Of course, this doesn’t prove that the virus can cause Parkinson’s, but the findings do seem to support an emerging picture of HCV as a neurotropic agent, or one that can affect nervous tissue. For instance, those chronically infected with HCV often show fatigue, depression, and even cognitive dysfunction, all of which are also symptoms of Parkinson’s. Furthermore, HCV genetic material has been recovered from the brains of deceased patients.

Interestingly this is not actually the first study to draw attention to this apparent association. In fact, it was only this year that another large study, albeit smaller with 62,000 subjects, found a significant link between Parkinson’s and HCV, but not HBV. That study actually went a bit further than the present investigation, and examined this potential relationship in the lab.

Using cultures of brain cells in a dish, the researchers discovered that HCV is capable of triggering the death of dopamine neurons; these are the cells that show progressive degeneration in Parkinson’s patients. Furthermore, they found that HCV can trigger the release of inflammatory molecules, which are also implicated in brain cell damage in Parkinson’s.

Clearly this link is worthy of further investigation, but if HCV becomes an established risk factor for Parkinson’s, this will have significant implications for public health, given that up to 150 million people are estimated to be chronically infected with the virus. Antiviral drugs can cure patients, but access to these medicines is low, especially in developing nations. And if HCV is indeed capable of damaging the nervous system, the burden of this virus is perhaps much more significant than previously believed. 

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