This episode examines the hepatitis viruses, a group of unrelated viruses unified by their shared target: the liver. Drawing from Murray’s Chapter 55, it explores how different genomic strategies converge on hepatocellular injury.

The episode is organised by virus:

* Hepatitis A virus (HAV) - non-enveloped RNA virus, faecal–oral transmission, acute self-limited disease

* Hepatitis B virus (HBV) - partially double-stranded DNA virus with reverse transcription step, blood and sexual transmission, chronic infection potential

* Hepatitis C virus (HCV) - enveloped RNA virus, high chronicity rate

* Hepatitis D virus (HDV) - defective RNA virus requiring HBV co-infection

* Hepatitis E virus (HEV) - faecal–oral transmission, severe disease in pregnancy

Pathogenesis involves immune-mediated hepatocyte injury rather than direct cytolysis alone. Chronic infection may lead to cirrhosis and hepatocellular carcinoma.

Conceptually, hepatitis viruses illustrate that organ tropism transcends viral taxonomy. Clinically, vaccination, antiviral therapy, and screening strategies are central to prevention and long-term management.

Key Takeaways

* Hepatitis viruses are genetically diverse but hepatotropic

* HAV and HEV are primarily faecal–oral

* HBV and HCV may become chronic

* Chronic infection increases cancer risk

* Vaccination is available for HAV and HBV

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