Viral hepatitis leads to liver cell apoptosis. A mononuclear inflammatory cell infiltrate extends from portal areas and disrupts the limiting plate of hepatocytes which are undergoing apoptosis, the so-called interface hepatitis of chronic active hepatitis. In this case, the hepatitis B surface antigen (HBsAg) and hepatitis B core antibody (HBcAb) were positive, but anti-HBs (seen with recovery) was negative. Presence of hepatitis B e antigen (HBeAg) is associated with an increased risk for hepatocellular carcinoma regardless of serum level of alanine aminotransferase (ALT).

The severity of infection relates to the immune system's ability to clear the virus. If clearance is delayed, a chronic persistent hepatitis can occur. A poor response can lead to chronic active hepatitis with ongoing hepatocellular damages and liver remodeling, with consequences of cirrhosis and potentially hepatocellular carcinoma.

Hepatitis B viral DNA can be measured by PCR. HBV DNA >2000 copies/mL along with an elevated alanine aminotransferase (ALT) suggests further workup and possible therapy is needed. Viral copies/mL above 10,000 suggest ongoing hepatitis with greater risk for carcinoma.

Pegylated interferon alfa (PEG-IFN-a), entecavir (ETV), and tenofovir disoproxil fumarate (TDF) are the agents primarily used for treatment of chronic active hepatitis B, suppressing, but not clearing the virus. Interferons have antiviral, antiproliferative, and immunomodulatory effects. Entecavir is a guanosine analogue inhibitor of hepatitis B viral polymerase. Tenofovir is a nucleotide analogue reverse transcriptase and HBV polymerase inhibitor.