Skip to content
PH-GI30

Hepatitis

How the hepatitis viruses A to E differ in spread and persistence, why the immune attack rather than the virus kills liver cells, how acute and chronic hepatitis look and are graded and staged, and how autoimmune and drug causes compare.

  • Free preview
  • 5 steps · 9 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Compare hepatitis viruses A to E by genome, route of spread, chronicity and prevention.
  • Explain why liver injury in viral hepatitis comes mainly from the immune response, and why the age at infection decides whether hepatitis B persists.
  • Describe the tissue picture of acute and chronic hepatitis, including interface hepatitis, portal lymphoid aggregates and ground-glass hepatocytes.
  • Distinguish grading from staging of chronic hepatitis, and interpret hepatitis B markers in general terms.
  • Explain autoimmune and drug-induced hepatitis, and how antivirals, vaccines and immunosuppression act on each mechanism.

What it is

Hepatitis is inflammation of the liver with injury to hepatocytes. It is acute when it settles within about six months and chronic when it lasts longer. The commonest causes worldwide are the five hepatitis viruses, A to E; others are autoimmune attack, drugs and toxins, alcohol and metabolic fatty liver disease.

4 types to tell apart
Acute viral hepatitis
Any of the five hepatitis viruses, and less often others such as Epstein–Barr virus and cytomegalovirus; most people recover completely.
Chronic viral hepatitis
Hepatitis B (with or without D) and C; hepatitis E only in people with weakened immunity. Years of inflammation can lead to cirrhosis and liver cancer.
Autoimmune hepatitis
An immune attack on hepatocytes with autoantibodies and raised IgG: type 1 (antinuclear and anti-smooth muscle antibodies) and type 2 (anti-LKM1, mostly in children).
Drug-induced hepatitis
Usually idiosyncratic; acute or, less often, chronic and autoimmune-like, and usually settling when the drug is stopped.

Normal function

Portal tracts, the limiting plate and a tolerant liver

Each carries a , a and a in a little connective tissue holding a few lymphocytes. The row of bordering the tract is the limiting plate, and the boundary between portal tract and lobule is the interface: the line chronic hepatitis attacks.

Portal blood brings a constant stream of harmless food and gut-bacterial antigens, so the liver is tolerant by default: and the sinusoid lining tend to damp immune responses rather than start them. Yet T cells passing along the sinusoids can touch hepatocytes directly through gaps in the lining, and hepatocytes display fragments of the proteins they make on MHC class I, so an infected hepatocyte can be found and killed.

Hepatitis viruses are hepatotropic: they enter hepatocytes through liver-specific receptors. Hepatitis B and D, for example, use NTCP, the transporter that takes bile acids back into hepatocytes. Hepatocytes regenerate readily, so if the cause is removed and the framework survives, even severe inflammation can heal without trace.

Point to it on the model