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The evolution of liver disease caused by chronic viral hepatitis, in particular the development of cirrhosis and hepatocellular carcinoma (HCC), is slow. As a consequence, clinicians have sought short-term, surrogate markers of disease progression as measures of treatment response.
In chronic hepatitis B virus (HBV) infection, suppression of serum HBV DNA below limits of detection and/or hepatitis B ‘e’ antigen (HBeAg) seroconversion have become the immediate goals of therapy. However, the pursuit of these treatment goals should not detract from the real treatment aims—the prevention of premature mortality from liver disease and/or the cure of chronic infection indicated by permanent hepatitis B surface antigen (HBsAg) seroconversion. Lying between these extremes in the hierarchy of goals would be the prevention of histological or clinical disease progression and, for patients with advanced disease, the induction of disease regression.
As experience with nucleos(t)ide analogues (NAs) grows and more effective treatments become available, the attainment of these goals in the treatment hierarchy has been achieved at increasingly higher levels. With the current generation of antivirals, the suppression of viral load below the limit of detection after 1 year of treatment is achievable in the great majority of patients.1–3 HBeAg seroconversion may be achieved in 30% of HBeAg positive patients after 4 years of treatment.4 Increasingly, loss of HBsAg is observed …