NATAP - DDW Liver Conference, San Diego, May 21-24 - Report 10

HCV AND THE BRAIN

At the recent EASL Conference, an oral presenter made the case that HIV enters the brain and that the brain may be a reservoir for HCV, as in the case of HIV. The researcher hypothesized that HCV may re-enter the blood or liver from the brain after being cleared by therapy. He also suggested that fatigue, depression and similar symptoms may be due to HCV entering the brain. At DDW, the following paper was presented.

COGNITIVE BRAIN FUNCTION IS SUBCLINICALLY IMPAIRED IN PATIENTS WITH CHRONIC HEPATITIS C - DOES HEPATITIS C AFFECT THE BRAIN?

Ludwig Kramer, Edith Bauer, Harald Hofer, Georg Funk, Petra Munda-Steindl, Christian Madl, Peter Ferenci, Dept of Medicine IV, Univ of Vienna, Vienna, Austria; Univ Hosp of Vienna, Vienna, Austria; Dept of Medicine IV, Vienna, Austria.

Fatigue and depression occur more frequently in chronic hepatitis C virus (HCV) infection than in other causes of chronic liver disease. However there is no correlation between severity of hepatitis and cerebral symptoms. It has been hypothesized that HCV exerted a direct effect on the brain. We studied the impact of HCV infection on sensitive markers of cognitive brain function. Fifty-eight noncirrhotic patients with chronic HCV infection (age, 45±13 years, mean±SD) were studied by P300 event-related potentials (an objective measure of cognitive processing) and by the SF-36 questionnaire for assessment of health-related quality of life. P300 latency is related to signal-processing speed; P300 amplitude reflects the amount of conscious attention paid to a stimulus. Findings were compared to 58 matched healthy subjects. We found that cognitive processing was subclinically impaired in patients (P300 latency: 361±38 ms, means±SD) as compared to healthy subjects (344±27 ms, p=0.01). Similarly, P300 amplitude was reduced in patients with HCV infection (12±7 vs. 18±7 µV, p<0.01). Health-related quality of life was significantly reduced in patients with HCV infection but there was no clear correlation between neurophysiological function and health-related quality of life or activity of hepatitis. In 7 out of 9 patients who were followed during antiviral combination treatment, P300 latency was improved after 12 weeks (345±29 ms) as compared to baseline (363±48 ms, p=0.08). In conclusion, patients with chronic HCV infection in the absence of cirrhosis exhibit a subclinical neurophysiological impairment. Cerebral function, however, seems to normalize with antiviral treatment. Our data might indicate a direct action of HCV infection on the brain. A theory that I've heard is that improvement from therapy is due to ribavirin because interferon does not enter the brain. But in HIV it's hypothesized that brain or cognivtive functioning may improve also because of improved immune function and not necessarily due only to direct antiviral drug affect in the brain or CNS.