Until recently the diagnosis of non-A, non-B hepatitis was made by excluding other detectable viral infections of the liver. Progress in molecular biology made it possible to develop assays which can trace antibodies against the hepatitis C virus. This virus plays a major role in the pathogenesis of transfusion-related and sporadic non-A, non-B hepatitis and possibly of other liver diseases. Although the genome of a few isolates of the hepatitis C virus has already been decoded, the viral particles have not yet been visualized.

Genome, Viral↗

PubMed1991

Surrogate markers are not useful for identification of HCV carriers in chronic hemodialysis patients.

Several diagnostic hepatitis C assays have been developed for the detection of antibodies to different antigens of the virus. This virus is the major cause of non-A, non-B hepatitis. Seventy-nine patients undergoing chronic hemodialysis and/or hemofiltration were tested for the presence of anti-HCV antibodies (anti-C-100-3 antibodies and anti-core antibodies), anti-hepatitis B core antibodies (anti-HBc), and aminotransferases (ALT). Seven patients were positive by one or more of the anti-HCV enzyme linked immunoassays (EIAs), while HCV-RNA was detectable in only four patients. These four patients had at least one, but not necessarily the same, positive anti-HCV EIA. HCV-RNA was not detected in patients who had no antibodies as determined by all six anti-HCV EIAs. All patients with a marker for HCV infection had persistent normal levels of transaminases. Three patients had elevated ALT values without a marker for HCV infection and suffered from hepatitis B virus infection. Anti-HBc was detected in 27/72 patients without any marker and in four patients with a marker of HCV infection. However, HCV-RNA was detectable in only one of these four anti-HBc positive patients. It is concluded that surrogate markers (anti-HBc and serum transaminases) are not useful for identification of HCV carriers in chronic hemodialysis patients.

Biomarkers↗

PubMed1990

Acetaldehyde selectively stimulates collagen production in cultured rat liver fat-storing cells but not in hepatocytes.

Hepatocytes and fat-storing cells have been implicated in the production of collagen, under both normal and pathological conditions. In this study, short-term primary cultures of rat hepatocytes, maintained in a serum-free, hormonally defined medium without dexamethasone and cultured on a fibronectin-collagen type IV substratum, were used. Primary and passage 1 and 2 cultures of fat-storing cells maintained on tissue culture plastic were also studied. Hepatocytes produced significant amounts of collagen type III, but formation of collagen type I was not detectable. Laminin and collagen type IV production were very low. Hepatocytes maintained their ability to metabolize ethanol (at levels comparable to those observed at 2 hr) for at least 48 hr after plating and this metabolism was inhibited 86% to 95% by 4-methylpyrazole (1 mmol/L). Neither ethanol (50 mmol/L) nor acetaldehyde (175 mumol/L, initial concentration) had any effect on the production of collagen type III or laminin. Fat-storing cells (95% to 100% desmin-positive) produced significant amounts of both type I and type III collagen. Production of collagen type IV and laminin was very low. Metabolism of ethanol by these cultures was not detected. Addition of ethanol had no effect on collagen or laminin production in fat-storing cells. In contrast, acetaldehyde significantly increased the production of collagen type I, but did not alter the production of collagen type III, IV or laminin. Incorporation of 3H-proline into total protein was not affected by addition of ethanol or acetaldehyde to fat-storing cells or hepatocytes. Exposure of fat-storing cells to ethanol or acetaldehyde did not change 3H-collagen degrading activity in the media.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗