About This Page
This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Transmitted via blood, sexual contact, vertical (mother-to-child). NOT faecal-oral (unlike hepatitis A and E)
- HBsAg positive >6 months = chronic hepatitis B. Most adults (>95%) clear acute infection; neonates only ~5% clear it
- Serology: HBsAg (current infection), anti-HBs (immunity), HBeAg (high infectivity), anti-HBc IgM (acute), HBV DNA (viral load)
- Chronic HBV treatment (if active): first-line antiviral = tenofovir or entecavir (nucleos(t)ide analogues)
- Lifelong HCC surveillance with 6-monthly USS ± AFP in patients with cirrhosis or significant fibrosis
Overview
Hepatitis B virus (HBV) is a partially double-stranded DNA virus of the Hepadnaviridae family. Transmission occurs via blood-borne, sexual, and vertical routes. Acute infection ranges from asymptomatic to fulminant hepatic failure. Chronic HBV (HBsAg positive >6 months) can lead to progressive hepatic fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The risk of chronicity is inversely related to age at acquisition: ~90% of neonatal infections become chronic versus <5% of immunocompetent adults. Phases of chronic HBV include immune-tolerant, immune-active (HBeAg-positive or negative), inactive carrier, and reactivation.
Epidemiology
Globally, approximately 296 million people have chronic HBV. In the UK, prevalence is relatively low (~0.3%), but higher in migrant communities from endemic areas (sub-Saharan Africa, East Asia, Eastern Europe). Universal neonatal HBV vaccination was introduced in the UK in 2017. Vertical transmission remains the most important route globally. The lifetime risk of HCC in chronic HBV is 15–25%, particularly if cirrhotic.
Clinical Features
Symptoms
Acute HBV: often asymptomatic. If symptomatic: malaise, anorexia, nausea, RUQ pain, jaundice (1–4 months post-exposure)
Arthralgia and urticarial rash (immune complex-mediated, prodromal phase)
Chronic HBV: usually asymptomatic until complications develop
Fatigue (common in chronic HBV)
Symptoms of decompensated liver disease: ascites, variceal bleeding, confusion
Signs
Jaundice (acute infection or decompensation)
Tender hepatomegaly (acute phase)
Signs of chronic liver disease: spider naevi, palmar erythema, gynaecomastia, splenomegaly
Polyarteritis nodosa (extrahepatic manifestation — small/medium vessel vasculitis, associated with HBV)
Signs of cirrhosis decompensation: ascites, jaundice, encephalopathy
Investigations
First-line
Hepatitis B serologyHBsAg (active infection), anti-HBs (immunity from vaccination or past infection), anti-HBc total (ever exposed), anti-HBc IgM (acute infection), HBeAg (high replication/infectivity), anti-HBe (lower replication)
HBV DNA viral load (PCR)Quantifies viral replication — guides treatment decisions. High viral load = active disease
LFTsALT (marker of hepatic inflammation — may be normal in immune-tolerant phase), bilirubin, albumin
Second-line
FibroScan (transient elastography)Non-invasive assessment of liver fibrosis — guides treatment decisions and HCC surveillance need
Hepatitis D co-infection screenTest for anti-HDV in all HBsAg-positive patients — HDV requires HBV for replication and accelerates liver damage
Hepatitis A immunity (anti-HAV)Vaccinate if non-immune (acute HAV on chronic HBV liver = higher risk of severe disease)
Specialist
Liver biopsyIf non-invasive assessment inconclusive — assess degree of inflammation and fibrosis (Ishak/METAVIR scoring)
6-monthly HCC surveillanceUSS ± AFP every 6 months in patients with cirrhosis, significant fibrosis, or family history of HCC
Management
NICE CG165 (Hepatitis B chronic), 20131
Acute hepatitis B
- Supportive: rest, hydration, avoid alcohol and hepatotoxic drugs
- Most immunocompetent adults clear infection spontaneously (>95%)
- Antivirals only if fulminant or severe prolonged acute infection
- Notify Public Health England (notifiable disease)
- Contact tracing and vaccination of household/sexual contacts
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Chronic hepatitis B — treatment indications
- Treat if: significant fibrosis/cirrhosis AND detectable HBV DNA, OR high HBV DNA (>2000 IU/mL) with raised ALT and/or significant fibrosis
- First-line antivirals: tenofovir disoproxil 245 mg OD or entecavir 0.5 mg OD (1 mg if lamivudine-resistant)
- Pegylated interferon-alpha (48-week course): considered in young, HBeAg-positive, high ALT, low HBV DNA — offers chance of finite treatment and HBsAg loss
- Treatment is usually long-term/lifelong with nucleos(t)ide analogues — stopping risks reactivation flare
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Monitoring (untreated)
- 6–12 monthly: ALT, HBV DNA, HBeAg/anti-HBe status
- FibroScan annually if active disease, 2-yearly if inactive carrier
- HCC surveillance USS every 6 months if cirrhotic or significant fibrosis
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Prevention
- Neonatal vaccination: universal UK schedule since 2017 (8, 12, 16 weeks as hexavalent vaccine)
- HBV immunoglobulin (HBIG) + vaccine within 24 hours of birth for babies of HBsAg-positive mothers
- Post-exposure prophylaxis: HBV vaccine ± HBIG depending on exposure type and vaccination status
- Condom use and safe injecting practice education
Complications
- Cirrhosis: Develops in 15–40% of untreated chronic HBV over 20+ years
- Hepatocellular carcinoma: Can occur even without cirrhosis (HBV DNA integrates into host genome). Lifetime risk 15–25%
- Fulminant hepatic failure: Rare (<1% of acute HBV) but life-threatening — higher risk with HDV co-infection
- HBV reactivation: With immunosuppression (rituximab, chemotherapy, steroids) — screen all patients before immunosuppressive therapy
- Extrahepatic: Polyarteritis nodosa, membranous nephropathy, aplastic anaemia
UKMLA Exam Tips
- 1HBsAg = SURFACE antigen = current infection. Anti-HBs = SURFACE antibody = immunity
- 2Anti-HBc IgM = ACUTE infection. Anti-HBc IgG = EVER been infected (present in chronic and resolved)
- 3Isolated anti-HBc positive: past infection (anti-HBs may have waned) — check HBV DNA to exclude occult HBV
- 4HBeAg positive = highly infectious (high replication). HBeAg negative + anti-HBe positive = lower replication (but pre-core mutants can still have high viral loads)
- 5Screen for HBV (HBsAg) BEFORE starting immunosuppressive therapy (especially rituximab, chemotherapy) — risk of fatal reactivation
- 6HBV can cause HCC WITHOUT cirrhosis — unique among hepatitis viruses (DNA integrates into genome)
- 7Vertical transmission prevention: HBIG + vaccine to neonate within 24 hours of birth
practicetest your knowledge on hepatitis bApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — gastroenterology and beyond.
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