Blood transfusion and hepatitis viruses
Transmission of hepatitis viruses has been recognised as an undesirable effect of blood transfusion since the 1940s, when large outbreaks occurred following inoculation with a yellow fever vaccine which contained pooled human plasma. Further reports followed of jaundice occurring several months after transfusions with blood or plasma. It was also noted in studies in the UK that the incidence of icteric hepatitis increased relative to the number of units transfused.
After the discovery of the Australia antigen in 1965, its recognition as a marker of hepatitis B virus (HBV) infection and its association with post-transfusion hepatitis (PTH), the subsequent introduction of screening tests for this antigen in the early 1970s led to a marked decrease in the incidence of PTH. However, despite increasingly sensitive testing methods for hepatitis B surface antigen (HBsAg), as it subsequently became designated, viral hepatitis was still considered the commonest lethal complication of blood transfusion. It was clear that there were still a number of cases of PTH that were due neither to hepatitis A virus nor to HBV, and the term 'non-A, non-B hepatitis' (NANBH) was coined.
The introduction of molecular techniques enabled clones to be derived from the genome of an agent associated with transfusion-transmitted NANBH, and the proteins derived from these clones were then used to develop nn enzyme linked immunosorbent assay (ELISA) to detect antibodies to this virus, now termed hepatitis C virus (HCV). This ELlSA is now used in most developed countries to screen for HCV antibodies.