{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T20:17:18Z","timestamp":1780517838779,"version":"3.54.1"},"reference-count":38,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2015,1,21]],"date-time":"2015-01-21T00:00:00Z","timestamp":1421798400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Viral Hepatitis"],"published-print":{"date-parts":[[2015,10]]},"abstract":"Summary<\/jats:title>Recent studies found that hepatitis C virus (HCV<\/jats:styled-content>) may invade the central nervous system, and both HCV<\/jats:styled-content> and Parkinson's disease (PD<\/jats:styled-content>) have in common the overexpression of inflammatory biomarkers. We analysed data from a community\u2010based integrated screening programme based on a total of 62\u00a0276 subjects. We used logistic regression models to investigate association between HCV<\/jats:styled-content> infection and PD<\/jats:styled-content>. The neurotoxicity of HCV<\/jats:styled-content> was evaluated in the midbrain neuron\u2013glia coculture system in rats. The cytokine\/chemokine array was performed to measure the differences of amounts of cytokines released from midbrain in the presence and absence of HCV<\/jats:styled-content>. The crude odds ratios (OR<\/jats:styled-content>s) for having PD<\/jats:styled-content> were 0.62 [95% confidence interval (CI<\/jats:styled-content>), 0.48\u20130.81] and 1.91 (95% CI<\/jats:styled-content>, 1.48\u20132.47) for hepatitis B virus (HBV<\/jats:styled-content>) and HCV<\/jats:styled-content>. After controlling for potential confounders, the association between HCV<\/jats:styled-content> and PD<\/jats:styled-content> remained statistically significant (adjusted OR<\/jats:styled-content>\u00a0=\u00a01.39; 95% CI<\/jats:styled-content>, 1.07\u20131.80), but not significantly different between HBV<\/jats:styled-content> and PD<\/jats:styled-content>. The HCV<\/jats:styled-content> induced 60% dopaminergic neuron death in the midbrain neuron\u2013glia coculture system in rats, similar to that of 1\u2010methyl\u20104\u2010phenylpyridinium (MPP<\/jats:styled-content>+<\/jats:sup>) but not caused by HBV<\/jats:styled-content>. This link was further supported by the finding that HCV<\/jats:styled-content> infection may release the inflammatory cytokines, which may play a role in the pathogenesis of PD<\/jats:styled-content>. In conclusion, our study demonstrated a significantly positive epidemiological association between HCV<\/jats:styled-content> infection and PD<\/jats:styled-content> and corroborated the dopaminergic toxicity of HCV<\/jats:styled-content> similar to that of MPP<\/jats:styled-content>+<\/jats:sup>.<\/jats:p>","DOI":"10.1111\/jvh.12392","type":"journal-article","created":{"date-parts":[[2015,1,21]],"date-time":"2015-01-21T19:25:01Z","timestamp":1421868301000},"page":"784-791","source":"Crossref","is-referenced-by-count":87,"title":["Hepatitis C virus infection: a risk factor for P<\/scp>arkinson's disease"],"prefix":"10.1111","volume":"22","author":[{"given":"W. 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