Clinical meaning
Viral hepatitis encompasses five major viruses (A through E) with distinct transmission routes, clinical courses, and management strategies. Hepatitis A (HAV) and E (HEV) are transmitted fecal-orally and cause self-limited acute hepatitis without chronic progression (mnemonic: vowels = bowel). Hepatitis B (HBV), C (HCV), and D (HDV) are blood-borne and can cause chronic hepatitis leading to cirrhosis and hepatocellular carcinoma (mnemonic: consonants = blood/body fluids). HBV is unique as the only DNA hepatitis virus (all others are RNA). HBV serology is complex but systematic: HBsAg indicates active infection (acute or chronic); anti-HBs indicates immunity (vaccine or resolved infection); IgM anti-HBc indicates acute infection; total anti-HBc indicates any prior exposure; HBeAg indicates high viral replication and infectivity. The 'window period' occurs when HBsAg has cleared but anti-HBs has not yet appeared — only IgM anti-HBc is positive during this period. HCV has no protective antibody; anti-HCV indicates exposure but requires HCV RNA quantification to confirm active infection (anti-HCV remains positive after cure). HCV is now curable with direct-acting antivirals (DAAs) achieving >95% sustained virologic response (SVR) in 8-12 weeks. HBV is controllable but rarely curable due to persistent cccDNA in hepatocyte nuclei. The clinician interprets hepatitis serology panels, determines chronicity versus acute infection, initiates antiviral therapy per guidelines, monitors treatment response, screens for HCC in at-risk patients, manages cirrhotic complications, and ensures appropriate vaccination and post-exposure prophylaxis.