Viral Hepatitis A, B, C, D, E & G
Description, Transmission and Causes of this Set of Viral Diseases
Jul 22, 2007
The existing viral hepatitis alphabet consists of hepatitis A, B, C, D, E and G. Their histories, in brief, are covered here.
Hepatitis A
In 1956 Dr Saul Krugman, a New York paediatrician, was asked to resolve a problem at the Willowbrook State School, Staten Island, an overcrowded home to 4,000 mentally disabled children, among whom hepatitis and other infectious diseases were rife. Krugman’s experiments involved both feeding and injecting infected blood into these children, and by the mid 1960s he had discovered two kinds of hepatitis, which would be later designated hepatitis A and hepatitis B. However, according to P. Radetsky's The Invisible Invaders: The Story of the Emerging Age of Viruses (1991), the ethics of Krugman’s experiments aroused controversy, and were subsequently censured by the New York Senate.
Hepatitis B
In 1963 Baruch Blumberg, a geneticist at New York’s Columbia medical school, found that the blood of some haemophilia patients contained antibodies which reacted with an antigen in the serum of an Australian aborigine. He called it the Australia antigen, known today as hepatitis B surface antigen (HBsAg), and showed that it is a marker for the presence of hepatitis B virus.
Hepatitis C
By 1975 laboratory tests to identify HAV and hepatitis B virus (HBV) infection became available, but by the 1980s it was clear that most cases of post-transfusion hepatitis were caused neither by HAV nor HBV. Originally referred to as non-A, non-B hepatitis, it is mainly caused by hepatitis C virus (HCV). In Hepatitis C Virus (Current Studies in Hematology and Blood Transfusion, no. 61) edited by Reesnik H.W. and published by Karger (1994), one finds that it was only after the application of molecular cloning techniques to the plasma of chimpanzees infected with non-A, non-B hepatitis that the HCV genome was finally identified in 1989.
Hepatitis D
In 1977, Dr Mario Rizetto, an Italian gastroenterologist, discovered hepatitis delta virus (HDV) while studying patients with chronic HBV infection. According to Jawetz, Melnick & Adelberg's Medical Microbiology (1991), published by Appleton & Lange, not all HBsAg-positive patients have HDV infection, but all patients with HDV infection are HBsAg positive and tend to have the most severe forms of acute and chronic hepatitis.
Hepatitis E
Dr K. Krawczynski, writing in a 1993 edition of Hepatology (17: 932), and entitled 'Hepatitis E', described how in New Delhi in 1955, almost 30,000 cases of icteric hepatitis occurred after faecal contamination of the drinking-water system. Originally thought to be caused by HAV, retrospective testing showed that neither HAV nor HBV were implicated. Hepatitis E virus (HEV) infection is typically associated with large waterborne epidemics in developing countries, and in the UK is usually seen only in patients who have returned from endemic areas.
Hepatitis G
With hepatitis viruses A to E established, the search for hepatitis F continued, with some researchers claiming they had found it — and then it seemed they hadn’t. In the ensuing confusion, when the next candidate hepatitis virus arose, it was decided, for clarity, not to designate it hepatitis F. In a 1997 article in volume 15 of Progress in Liver Diseases, and entitled 'The hepatitis G virus: biology, epidemiology, and search for disease', Dr S.J. Hadziyannis begins in the 1960s, when a 34-year-old surgeon (initials GB) from Chicago developed acute hepatitis of unknown origin. When monkeys were injected with GB’s serum, they later showed evidence of hepatitis. However, the GB agent received no more attention until 1995, when researchers at Abbott Laboratories began working with stored monkey serum samples from the original GB experiments and isolated a virus they termed GBV-C. Yet they failed to detect GBV-C in GB’s stored serum. But meanwhile, independently, a group working for Genelabs Technologies identified a virus in the plasma of a patient with chronic hepatitis and named it HGV. It is now recognised that GBV-C and HGV are independent isolates of the same virus.
