{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,29]],"date-time":"2025-09-29T15:34:31Z","timestamp":1759160071387,"version":"3.30.0"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":5417,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2000,11]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>As a part of the defense mechanism of the host to viral infection, interferons induce the transcription of several genes. These interferon\u2013inducible genes contribute to the eradication of the viruses. Whereas some studies suggested the participation of a dsRNA\u2013dependent protein kinase in the host reaction to hepatitis C virus infection, the involvement of other interferon\u2013inducible genes has not been evaluated. Furthermore, there has been no analysis on the expression profile of multiple interferon\u2013inducible genes. The aim of this study was to clarify the hepatic mRNA expression profile of interferon\u2013inducible genes with a special concern to chronic hepatitis C. A total of 76 liver biopsy samples (28 with chronic hepatitis C, 10 with chronic hepatitis B, 9 with alcoholic liver disease, 14 with autoimmune hepatitis, 10 with primary biliary cirrhosis, and 5 of normal liver) were enrolled. The expression of the following genes was quantified by competitive reverse transcription\u2013polymerase chain reaction and was compared according to the etiology; dsRNA\u2013dependent protein kinase (PKR), 2\u2032,5\u2032\u2013oligoadenylate synthetase (2,5\u2013AS), latent cellular endoribonuclease (RNase L), RNase L inhibitor, and MxA. As a result, PKR mRNA was significantly overexpressed in the liver of chronic hepatitis C compared with those of other etiologies (<jats:italic toggle=\"yes\">P<\/jats:italic>= .0178), and it correlated significantly with serum alanine transaminase values (r = .51, <jats:italic toggle=\"yes\">P<\/jats:italic> = .0054). Also, the expression of the RNase L inhibitor showed a significant reduction in chronic hepatitis C (<jats:italic toggle=\"yes\">P<\/jats:italic> = .0184). The expressions of 2,5\u2013AS, RNase L, and MxA were not different significantly irrespective to the etiology. In conclusion, hepatic overexpression of PKR and reduced expression of RNase L inhibitor seem to contribute to the anti\u2013HCV mechanism characteristically.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1053\/jhep.2000.19287","type":"journal-article","created":{"date-parts":[[2003,6,21]],"date-time":"2003-06-21T14:16:51Z","timestamp":1056205011000},"page":"1089-1095","update-policy":"http:\/\/dx.doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":27,"title":["Intrahepatic Mrna Expression of Interferon\u2013Inducible Antiviral Genes in Liver Diseases: Dsrna\u2013Dependent Protein Kinase Overexpression and Rnase L Inhibitor Suppression in Chronic Hepatitis C"],"prefix":"10.1097","volume":"32","author":[{"given":"Shin-Han","family":"Yu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazuyoshi","family":"Nagayama","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nobuyuki","family":"Enomoto","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Namiki","family":"Izumi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fumiaki","family":"Marumo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chifumi","family":"Sato","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"10.1053\/jhep.2000.19287-BIB1","doi-asserted-by":"crossref","first-page":"5017","DOI":"10.1016\/S0021-9258(18)42719-6","volume":"267","author":"Sen","year":"1992","journal-title":"J 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