Viral Hepatitis
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Direct answer
Viral hepatitis is hepatocellular injury from hepatotropic viruses — A, B, C, D and E — differing in transmission, chronicity and serology. Faecal-oral A and E cause self-limited acute hepatitis, except that E is fulminant in pregnancy. Blood-borne B and C produce acute disease that may persist: hepatitis B runs a defined antigen-antibody choreography — HBsAg, HBeAg, anti-HBc with its IgM window-period signal and anti-HBs recovery marker — while hepatitis C becomes chronic, mostly silently, in the majority of patients, leading to cirrhosis and hepatocellular carcinoma. Histologically, acute hepatitis shows ballooning degeneration, apoptotic Councilman bodies and lobular inflammation, while chronic disease adds interface hepatitis with progressive fibrosis.
What you must remember
- Hepatitis A: RNA picornavirus, faecal-oral spread, short incubation, IgM anti-HAV confirms acute infection; never chronic; vaccine preventable.
- Hepatitis B: DNA hepadnavirus spread by blood, sexual contact and vertical transmission; HBsAg appears first, anti-HBc IgM marks acute infection and covers the window period when HBsAg has cleared but anti-HBs has not appeared; anti-HBs means recovery or vaccination; HBeAg and HBV DNA indicate high infectivity; chronicity in most neonates but few adults.
- Hepatitis C: RNA flavivirus, blood-borne; acute infection is usually silent, but most patients develop chronic hepatitis; cirrhosis and hepatocellular carcinoma follow; anti-HCV screens and HCV RNA confirms; direct-acting antivirals cure the great majority per current guidance; no vaccine.
- Hepatitis D: defective RNA virus needing HBsAg to replicate; superinfection of a chronic carrier causes the severest disease with fulminant risk.
- Hepatitis E: RNA virus, faecal-oral, water-borne outbreaks in India; fulminant hepatitis with high mortality in third-trimester pregnancy; chronic infection possible in immunosuppression.
- Acute hepatitis histology: hepatocyte swelling (ballooning), apoptosis as acidophilic Councilman bodies, lobular disarray with Kupffer cell hyperplasia, portal inflammation and cholestasis.
- Chronic hepatitis and severity: portal lymphocytic inflammation with interface (piecemeal) necrosis, bridging necrosis and staged fibrosis toward cirrhosis; confluent or submassive necrosis underlies fulminant hepatic failure.
Common confusion
Window-period questions decide ranks: when HBsAg is negative and anti-HBs is absent, IgM anti-HBc is the only positive marker. Isolated anti-HBs means vaccine; anti-HBs plus IgG anti-HBc means recovered infection; HBsAg beyond six months means chronicity. IgM versus IgG anti-HAV or anti-HBc separates fresh from remote infection. Students also conflate HCV antibody — evidence of exposure, needing RNA to confirm active infection — with immunity, which it is not.
Exam-focused takeaway
Serology grids dominate: match marker panels to phases, interpret the pregnant woman with jaundice and high mortality risk (hepatitis E), or the chronic carrier superinfected with hepatitis D. Histology one-liners test Councilman bodies, piecemeal necrosis and bridging necrosis. Keep transmission, chronicity and mortality risk sorted per virus — the three axes every grid question uses.
Frequently asked questions
What appears during the window period of hepatitis B?
IgM anti-HBc alone, after HBsAg has declined and before anti-HBs has risen.
Which hepatitis virus is deadliest in pregnancy?
Hepatitis E, causing fulminant hepatic failure with high mortality in the third trimester.
How is hepatitis C diagnosis confirmed?
Anti-HCV screening followed by HCV RNA testing to prove active infection, since antibody alone reflects exposure.
What are Councilman bodies?
Shrunken, eosinophilic apoptotic hepatocytes extruded into sinusoids — the histological signature of acute viral hepatitis.
What is interface hepatitis?
Extension of chronic inflammatory cells from portal tracts into the parenchyma with hepatocyte death (piecemeal necrosis), the lesion that drives fibrosis toward cirrhosis.