Apolipoprotein E‐ε4 deficiency and cognitive function in hepatitis C virus‐infected patients. Issue 1 (26th August 2015)

• Record Type: Journal Article
• Authors: Wozniak, M. A.; Lugo Iparraguirre, L. M.; Dirks, M.; Deb‐Chatterji, M.; Pflugrad, H.; Goldbecker, A.; Tryc, A. B.; Worthmann, H.; Gess, M.; Crossey, M. M. E.; Forton, D. M.; Taylor‐Robinson, S. D.; Itzhaki, R. F.; Weissenborn, K.
• Is Part Of: Journal of viral hepatitis. Volume 23:Issue 1(2016)
• Page Start: 39
• Page End: 46
• Publication Date: 2015-08-26
• Subjects: attention -- cerebral lipoprotein metabolism -- hepatitis C virus encephalopathy -- neurodegeneration -- virus replication; Hepatitis, Viral -- Periodicals; Hepatitis, Viral, Animal; Hepatitis, Viral, Human; 616.3623
• DOI: 10.1111/jvh.12443
• Languages: English
• ISSNs: 1352-0504

Abstract

Summary: Hepatitis C virus (HCV) causes not only liver damage in certain patients but can also lead to neuropsychiatric symptoms. Previous studies have shown that the type 4 allele of the gene for apolipoprotein E (APOE) is strongly protective against HCV‐induced damage in liver. In this study, we have investigated the possibility that APOE genotype is involved in the action of HCV in brain. One hundred HCV‐infected patients with mild liver disease underwent a neurological examination and a comprehensive psychometric testing of attention and memory function. In addition, patients completed questionnaires for the assessment of fatigue, health‐related quality of life and mood disturbances. Apolipoprotein E gene genotyping was carried out on saliva using buccal swabs. The APOE‐ε4 allele frequency was significantly lower in patients with an impairment of working memory, compared to those with a normal working memory test result ( P = 0.003). A lower APOE‐ε4 allele frequency was also observed in patients with definitely altered attention ability ( P = 0.008), but here, the P ‐value missed the level of significance after application of the Bonferroni correction. Our data suggest that the APOE‐ε4 allele is protective against attention deficit and especially against poor working memory in HCV‐infected subjects with mild liver disease. Considering the role of apolipoprotein E in the life cycle of the virus, the findings shed interesting new light upon possible pathomechanisms behind the development of neuropsychiatric symptoms in hepatitis C infection.