A long-term study of hepatitis C virus replication in non-A, non-B hepatitis

Article Abstract:

Cases of viral hepatitis which could not be demonstrated to be either hepatitis A or hepatitis B have traditionally been lumped together as non-A, non-B hepatitis. While not all such cases have the same cause, the majority of non-A, non-B hepatitis cases which occur after a patient has received a blood transfusion are now known to be caused by another virus, appropriately named hepatitis C virus (HCV). Until recently, little has been known about this virus or the natural history of the infection it causes. However, recently the genes of this virus have been cloned, which provides a valuable tool for researchers probing the course of hepatitis C infection. These tools have now been employed in the study of the course of hepatitis C infection. The highly sensitive polymerase chain reaction (PCR) was used to detect the presence of hepatitis C virus genes in samples of blood serum from five patients with post-transfusion hepatitis. The same method was used to follow the experimental infection of chimpanzees with serum from four of the patients. These samples covered not only the acute infection, but also from 10 to 14 years of patient follow-up. The results demonstrated that the levels of antibodies to hepatitis C virus were not good indicators of the infectious process. During the first several months of the infection, no antibodies could be detected and viral genes in the blood serum were the only markers of infection. One patient had only acute hepatitis which resolved spontaneously; the resolution of symptoms in this patient correlated with the disappearance of viral genes from the blood. Antibodies to HCV, however, persisted for nine years. The remaining four patients developed chronic hepatitis, which was active in three cases. In these patients, persistence of virus in the body could be demonstrated using the PCR technique. These results demonstrate that the measurement of antibodies to hepatitis C virus is not a reliable indicator of the state of infection. (Consumer Summary produced by Reliance Medical Information, Inc.)

Genetic aspects, Hepatitis, Viral, Viral hepatitis, Observations

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Detection of antibody to hepatitis C virus in prospectively followed transfusion recipients with acute and chronic non-A, non-B hepatitis

Article Abstract:

Until recently, standard detection procedures for non-A, non-B hepatitis have not been available and a definitive confirmation of the diagnosis has remained difficult. One of the consequences of this has been a seven to 12 percent chance of contracting hepatitis from a blood transfusion. Serious long-term complications may result from this infection, which include chronic hepatitis and cirrhosis of the liver, and there is a possible connection with liver cancer. A method to study the non-A, non-B hepatitis virus has been devised by the cloning or genetic duplication of an agent which has been designated hepatitis C (HCV). A test was developed to detect the antibody that is produced in response to this agent; additional tests that are specific for anti-HCV antibodies have also been developed. Fifteen individuals who had received a blood transfusion and subsequently developed non-A, non-B hepatitis were followed for several years, as were their donors. A radioactive assay for anti-HCV antibodies was performed and compared with selected samples of blood with transfusion-associated hepatitis. Anti-HCV was detectable in 14 subjects or 88 percent of these recipients with traceable donors. Hepatitis C virus was found to be the primary agent of non-A, non-B transfusion-associated hepatitis. The researchers concluded that if blood donors were screened for anti-HCV, most cases of transfusion-associated hepatitis could be prevented.

Prevention, Blood transfusion, Viral antibodies, Hepatitis E

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Hepatitis C virus-associated fulminant hepatic failure

Article Abstract:

The hepatitis C virus (HCV) may be capable of causing liver failure. This was discovered when a 68-year-old man was admitted to a hospital for coronary artery bypass surgery. He had no history of liver disease. He received blood transfusions during surgery. He was admitted again one month later with signs of liver disease and died 11 days later of liver failure. Blood samples taken before and after surgery were negative for HCV but turned positive 5 weeks later. Liver samples taken at autopsy tested positive for HCV.

Liver failure

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