VIRAL MARKERS IN THE TREATMENT OF HEPATITIS-B AND HEPATITIS-C

Acute hepatitis B virus (HBV) infection is typically distinguished fro m chronic disease by a positive IgM anti-hepatitis B core antigen (ant i-HBc) test. Patients with chronic hepatitis B remain hepatitis B surf ace antigen (HBsAg) positive, often with raised serum alanine aminotra nsferase (ALT) activities, for more than six months. The presence of h epatitis B e antigen (HBeAg) and HBV-DNA correlates with infectivity ( although patients infected with the pre-core mutated virus may be HBeA g negative). Immunity after HBV infection is characterised by the pres ence of anti-HBs and anti-HBc antibodies. Patients who respond to inte rferon alfa treatment lose HBV-DNA and HBeAg from serum and their ALT values return to normal; some also lose HBsAg and acquire anti-HBs. Di agnosis of acute hepatitis C virus (HCV) infection remains largely dep endent on history and exclusion, as anti-HCV antibodies may appear lat e or never at all, although HCV-RNA may be detectable on polymerase ch ain reaction (PCR) within days of infection. Second generation ELISAs detect a range of anti-HCV antibodies in chronic infections, and confi rmatory RIBAs have reduced the incidence of false-positive results. Di rect tests for HCV antigens in serum are not yet available, although P CR testing for HCV-RNA can be used to confirm viraemia. Patients who r espond to interferon alfa treatment show continuous normalisation of s erum ALT values, and some lose HCV-RNA. Relapse occurs in about half o f all those who respond.