🦠 Hepatitis B virus (HBV) is a highly infectious, partially double-stranded DNA virus that infects hepatocytes.
It may cause acute hepatitis, chronic hepatitis, cirrhosis and hepatocellular carcinoma.
The most important concepts are: HBsAg = current infection, anti-HBc IgM = acute/recent infection, and anti-HBs = immunity.
ℹ️ About
🧬 HBV is a partially double-stranded DNA virus from the Hepadnaviridae family.
🌍 It is endemic in parts of sub-Saharan Africa, East Asia, the Pacific, the Middle East and Eastern Europe.
🇬🇧 In the UK, many cases are diagnosed in people born in higher-prevalence countries or in people with blood-borne virus risk factors.
⚠️ Many people are asymptomatic, so infection may be found incidentally on screening or abnormal liver blood tests.
🎗 Chronic HBV can lead to cirrhosis and hepatocellular carcinoma, even when symptoms are minimal.
💉 HBV is vaccine-preventable.
🩸 Transmission
🩸 Blood exposure: needle sharing, injecting drug use, needlestick injury, non-sterile tattooing/piercing, or healthcare exposure in high-prevalence settings.
👶 Vertical transmission: mother to baby, especially if the mother has high HBV DNA or is HBeAg positive.
❤️ Sexual transmission: unprotected sex with an infected partner.
🏠 Household transmission: sharing razors or toothbrushes where blood exposure may occur.
🚫 HBV is not spread by casual contact, hugging, sharing food, coughing or breastfeeding if the baby has received appropriate prophylaxis.
🧬 Virology & Key Markers
HBsAg: hepatitis B surface antigen; marker of current infection.
HBcAg: hepatitis B core antigen; not usually measured directly in blood.
HBeAg: marker associated with high viral replication and infectivity.
Anti-HBs: antibody to surface antigen; indicates immunity after recovery or vaccination.
Anti-HBc IgM: marker of acute or recent natural infection.
Anti-HBc IgG / total anti-HBc: marker of previous natural exposure; not produced by vaccination.
Anti-HBe: often suggests lower infectivity, but HBV DNA is more reliable.
HBV DNA: direct viral load; used to assess replication, infectivity and treatment response.
📈 Hepatitis B Serology Over Time
🦠 Hepatitis B serology changes predictably after infection.
HBsAg appears first and indicates current infection.
Anti-HBc IgM suggests recent acute infection and is the key marker during the window period.
Anti-HBs appears after recovery or vaccination and usually indicates immunity.
🧪 Marker Interpretation
Marker
Meaning
Exam clue
HBsAg
Surface antigen; indicates current HBV infection, either acute or chronic.
If present for >6 months → chronic HBV.
Anti-HBs
Antibody to surface antigen; indicates immunity after recovery or vaccination.
Only anti-HBs positive = vaccinated immunity.
Anti-HBc IgM
IgM antibody to core antigen; suggests acute or recent infection.
Key marker in the window period.
Anti-HBc IgG / total anti-HBc
Indicates previous natural exposure to HBV.
Positive in past infection and chronic infection; not produced by vaccination.
HBeAg
Marker associated with high viral replication and infectivity.
Higher transmission risk, especially in pregnancy.
Anti-HBe
Often suggests lower viral replication.
HBV DNA is more reliable than anti-HBe alone.
HBV DNA
Direct measure of viral replication.
Used for infectivity, treatment decisions and monitoring response.
🧩 Common Serology Patterns
HBsAg
Anti-HBs
Anti-HBc
Likely interpretation
−
−
−
Susceptible: no evidence of infection or immunity.
−
+
−
Immune due to vaccination.
−
+
+
Immune due to past natural infection.
+
−
IgM +
Acute HBV infection.
+
−
IgG / total +
Chronic HBV if HBsAg persists for >6 months.
−
−
IgM +
Window period of acute infection.
−
−
Total +
Isolated core antibody: previous infection, false positive, resolving infection, or occult HBV. Check HBV DNA if relevant.
🩺 Clinical Course
⏱ Incubation is usually 2–6 months.
Acute infection: often asymptomatic; may cause fever, malaise, nausea, anorexia, rash, arthralgia, jaundice, dark urine and raised ALT/AST.
Fulminant hepatitis: rare but life-threatening; suspect if jaundice, coagulopathy, encephalopathy or severe systemic illness.
Chronic infection: defined by HBsAg persistence for more than 6 months.
Chronicity risk: highest after perinatal infection, lower after adult-acquired infection.
Complications: cirrhosis, hepatic decompensation and hepatocellular carcinoma.
🚩 Risk Factors for Chronic Infection
👶 Vertical transmission or infection in infancy.
🧒 Infection in early childhood.
🛡 Immunosuppression, including chemotherapy, transplantation or advanced HIV.
🧬 Male sex and family/genetic factors may influence disease course.
🦠 Co-infection with HDV, HCV or HIV may worsen outcomes.
🔎 Who to Test
People born in or with parents from high-prevalence countries.
Sexual partners and household contacts of people with HBV.
People who inject drugs or share injecting equipment.
People with HIV, hepatitis C, hepatitis D risk, or other blood-borne virus risk factors.
People with unexplained abnormal liver blood tests.
Pregnant women as part of antenatal screening.
Healthcare workers and people after occupational exposure.
Dialysis patients, transplant recipients and people needing immunosuppression or chemotherapy.
🧪 Investigations
Initial serology: HBsAg and anti-HBc as a minimum; anti-HBs helps assess immunity.
If HBsAg positive: HBV DNA, HBeAg, anti-HBe, LFTs, albumin, INR, FBC and renal function.
Screen for co-infection: HIV, hepatitis C and hepatitis D.
Fibrosis assessment: transient elastography, serum fibrosis markers or specialist assessment.
HCC surveillance: ultrasound surveillance if cirrhosis or high-risk chronic HBV, guided by hepatology.
Before immunosuppression: check HBV serology because HBV can reactivate with chemotherapy, biologics and high-dose steroids.
💊 Management - Acute Hepatitis B
Supportive care: most immunocompetent adults clear acute HBV spontaneously.
🍷 Avoid alcohol during acute hepatitis.
💊 Avoid unnecessary hepatotoxic drugs.
🚑 Admit urgently if jaundice with coagulopathy, encephalopathy, severe vomiting, dehydration, sepsis, or suspected acute liver failure.
👨⚕️ Discuss severe acute HBV with hepatology; antivirals may be needed in severe or fulminant disease.
🧪 Follow-up serology is required to confirm clearance or progression to chronic infection.
💊 Management - Chronic Hepatitis B
Specialist-led: chronic HBV should be assessed and monitored by hepatology or an infectious diseases/liver specialist.
Treatment decisions depend on: HBV DNA, ALT, HBeAg status, fibrosis stage, cirrhosis, age, family history of HCC and comorbidities.
Antivirals: tenofovir disoproxil, tenofovir alafenamide or entecavir are commonly used potent nucleos(t)ide analogues.
Pegylated interferon-alpha: may be considered in selected patients but is less commonly used than oral antivirals.
Cirrhosis: usually requires antiviral therapy if HBV DNA is detectable, plus cirrhosis surveillance and complication management.
Monitoring: ALT, HBV DNA, renal function, bone risk where relevant, fibrosis progression and HCC surveillance if indicated.
Liver transplant: considered for end-stage liver disease or selected cases of HCC.
🤰 Pregnancy & Newborn Prevention
All pregnant women should be screened for HBsAg.
If the mother is HBsAg positive, assess infectivity with HBeAg and HBV DNA.
High maternal viral load increases the risk of vertical transmission.
Babies born to HBsAg-positive mothers need hepatitis B vaccination starting within 24 hours of birth.
Babies at higher risk, such as those born to highly infectious mothers, may also need hepatitis B immunoglobulin.
Ensure follow-up infant testing to confirm whether infection has been prevented.
💉 Prevention
Vaccination: safe and effective; part of the UK routine childhood programme and offered to high-risk groups.
Post-exposure prophylaxis: risk-assess needlestick and sexual exposures; may require accelerated vaccination ± HBIG.
Contacts: test and vaccinate household and sexual contacts where appropriate.
Sexual health: condoms and partner notification/testing.
Healthcare workers: vaccination and post-vaccination anti-HBs testing according to occupational health guidance.
📝 Exam Pearls
🦠 HBsAg positive = current infection.
⏳ HBsAg positive for >6 months = chronic hepatitis B.
🧪 Anti-HBc IgM = acute/recent infection and the key marker in the window period.
💉 Anti-HBs only = vaccination response.
🧬 Anti-HBc means natural exposure; vaccination does not produce anti-HBc.
🔥 HBeAg and HBV DNA suggest higher infectivity and replication.
🤰 Vertical transmission is more likely if maternal HBV DNA is high or HBeAg is positive.
🦠 Always consider HDV testing in HBsAg-positive patients, especially if severe disease or risk factors are present.
🧠 Teaching Note
Think of HBV serology as a story in three stages: virus arrives, immune system responds, immunity appears.
HBsAg appears early because viral surface antigen is circulating in the blood, while anti-HBc IgM appears when the immune system recognises true natural infection.
During the window period, HBsAg has disappeared but anti-HBs has not yet appeared, so anti-HBc IgM may be the only positive marker.
Vaccination produces anti-HBs without anti-HBc because the vaccine contains surface antigen, not core antigen.
