Does hepatitis C virus play a role in "non-viral" chronic liver disease?
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Updated: Oct 2, 2026

A Protocol for Analyzing Hepatitis C Virus Replication
Published on: June 26, 2014
C Liddle1, E B Crewe, N R Swanson
1University of Sydney, NSW.
Insights
Hepatitis C virus (HCV) antibodies were detected in some patients with unexplained liver disease, suggesting HCV may cause cryptogenic cirrhosis. However, HCV is unlikely to cause autoimmune liver diseases.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Chronic liver diseases are often attributed to non-viral causes.
- The role of hepatitis C virus (HCV) in these conditions is under investigation.
Purpose of the Study:
- To investigate the presence of anti-HCV antibodies in patients with chronic liver diseases of unknown etiology.
- To determine if HCV infection contributes to conditions like cryptogenic cirrhosis and autoimmune chronic active hepatitis.
Main Methods:
- Sera from 140 patients with
- non-viral
- chronic liver diseases, 51 with chronic non-A, non-B (NANB) hepatitis, and 25 with non-hepatic autoimmune disorders were tested for anti-HCV antibodies.
- Patients were assessed for risk factors for parenteral transmission.
Main Results:
- 88% of chronic NANB hepatitis patients were anti-HCV seropositive.
- 8 out of 26 patients (31%) with cryptogenic cirrhosis were anti-HCV seropositive, with 5 having no clear transmission risk.
- Only 4.7% of other chronic liver disease patients without known risk factors tested positive for anti-HCV.
Conclusions:
- Hepatitis C virus infection may be a cause of some cryptogenic cirrhosis cases.
- The low prevalence of anti-HCV in autoimmune chronic active hepatitis suggests HCV is not a primary cause of this condition.
Abstract:
It has recently been suggested that the hepatitis C virus may play a significant role in chronic liver diseases, such as autoimmune chronic active hepatitis, which are usually attributed to non-viral causes. We tested for antibodies to hepatitis C virus (anti-HCV) in sera from 140 patients with well characterised "non-viral" chronic liver diseases as well as sera from 51 patients thought to have chronic non-A, non-B (NANB) hepatitis (acting as positive controls) and 25 patients with non-hepatic autoimmune disorders. As expected, 45 of 51 patients (88%) diagnosed as having chronic NANB hepatitis were anti-HCV seropositive. Among 26 patients with cryptogenic cirrhosis, 8 were anti-HCV seropositive; in 5 patients (22%) there was no apparent risk factor for parenteral transmission. In the remaining 114 patients with chronic liver disease, 10 patients (9%) were seropositive for anti-HCV. However, 5 of these patients had a significant risk factor for parenteral transmission of hepatitis C virus, leaving only 5 of 106 (4.7%) with unexplained positive anti-HCV test results. Among patients with high titres of circulating autoantibodies but no liver disease, no positive results occurred. It is concluded that hepatitis C virus infection may account for some cases of cryptogenic cirrhosis. Although anti-HCV occurs more commonly in patients with other "non-viral" chronic liver diseases than has been reported in the community (0.5%-1.2%), the low prevalence of the antibodies indicates that hepatitis C virus infection is unlikely to be important in the aetiology or pathogenesis of autoimmune chronic active hepatitis and other poorly understood chronic liver diseases.
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