Haemolysis in hepatitis A virus infections coinciding with the occurrence of autoantibodies against triosephosphate isomerase and the reactivation of latent persistent Epstein-Barr virus infection.

Haemolysis has been observed frequently as a complication of acute hepatitis A virus (HAV) infection. However, the pathogenic mechanism has not been elucidated completely. In individual cases the detection of anti-erythrocyte antibodies of unknown specificity was described. The raised serum IgM fraction was shown to consist partially of autoantibodies. Previously, we detected autoantibodies of immunoglobulin class M directed against triosephosphate isomerase (IgM anti-TPI) in patients with infectious mononucleosis. These autoantibodies are able to induce haemolysis. In this study the occurrence of IgM anti-TPI in acute HAV infections and other viral diseases has been investigated. In 33 of 134 patients suffering from HAV infection (IgM anti-TPI was detected. Haematological and chemical data were available from seven of these 33 patients. Mild-to-moderate signs of haemolysis correlating with the IgM anti-TPI titre in the follow-up examinations were demonstrated. The presence of IgM anti-TPI in HAV infections is connected with a reactivation of a latent persistent EBV infection. In other viral infections both the detection of IgM anti-TPI and evidence of a reactivated EBV infection is rare. Thus, we anticipate that IgM anti-TPI antibodies occurring with the reactivation of a latent persistent EBV infection take part in provoking haemolysis in acute HAV infections.