Abstract
The risk of hepatitis virus transmission from transfusions has declined dramatically from that of the 1940s when posttransfusion hepatitis (PTH) was first appreciated. Introduction of hepatitis B surface antigen screening and conversion to volunteer donors for whole-blood donations in the late 1960s and early 1970s led to substantial reduction in PTH cases. However, up to 10% of the recipients continued to develop PTH, most cases of which were attributed to an unknown non-A, non-B viral agent. Implementation of surrogate marker testing (i.e., alanine aminotransferase and anti-hepatitis B virus core antigen) for residual non-A, non-B hepatitis in the late 1980s reduced the per unit risk of PTH from 1 in 200 to about 1 in 400. Hepatitis C virus was discovered in 1989 and quickly was established as the causative agent of >90% of non-A, non-B PTH. Introduction of progressively improved antibody assays in the early 1990s reduced the risk of PTH due to hepatitis C virus to about 1 in 100 000. Although additional hepatitis viruses exist (e.g., hepatitis G virus), these appear to be minor contributors to clinical PTH, which has been virtually eradicated.
Detection of antibody against antigen expressed by molecularly cloned hepatitis C virus cDNA: application to diagnosis and blood screening for posttransfusion hepatitis.
