Chronic hepatitis B

Chronic hepatitis B: the Australian general practice management guide

Chronic hepatitis B (CHB) is infection with hepatitis B virus persisting more than six months. Around 230,000 Australians live with CHB, and approximately 40% remain undiagnosed. High-prevalence groups include migrants from Asia, the Pacific Islands, and sub-Saharan Africa, and Aboriginal and Torres Strait Islander Australians.

Treatment is not always needed but is highly effective when indicated — tenofovir or entecavir suppress the virus and reduce liver cancer risk. GPs with Section 100 accreditation can prescribe these antivirals in general practice. Vaccination prevents infection and is universal under the National Immunisation Program.

Chronic hepatitis B (CHB) is the most common chronic viral infection of the liver worldwide, and Australia has a substantial but largely hidden burden. Around 230,000 Australians live with CHB, yet approximately 40% remain undiagnosed. This diagnostic gap is where general practice makes the biggest difference — identifying people from high-prevalence groups, offering testing, and connecting them to lifelong monitoring and treatment where needed.

CHB can lead to cirrhosis, liver failure, and hepatocellular carcinoma (HCC). Crucially, HCC can develop even without cirrhosis — particularly in Asian-ancestry men, Aboriginal and Torres Strait Islander Australians, and people with a family history of liver cancer. This is why surveillance is based on age, ancestry, and family history, not cirrhosis status alone.

The good news is that current antivirals — tenofovir, tenofovir alafenamide, and entecavir — suppress hepatitis B virus to undetectable levels in the vast majority of treated patients, dramatically reducing the risks of disease progression and liver cancer. An important feature of the Australian healthcare system is Section 100 community prescribing, which enables accredited GPs to prescribe these medications directly, reducing specialist bottlenecks for stable patients.

A. Core clinical — the AU general practice framework

Who to screen

High-prevalence groups that should receive CHB serology (HBsAg, anti-HBc total, anti-HBs) regardless of symptoms:

  • Migrants from Asia (including South and South-East Asia), Pacific Islands, and sub-Saharan Africa — CHB prevalence 5–10% in these communities
  • Aboriginal and Torres Strait Islander people — prevalence 3–4%
  • People who inject drugs
  • Men who have sex with men
  • Sex workers and prisoners
  • People living with HIV or hepatitis C
  • Household contacts and sexual partners of people with CHB
  • People born to HBsAg-positive mothers (vertical transmission)
  • Healthcare workers without documented immunity

CHB testing is a standard component of the MBS-funded Aboriginal and Torres Strait Islander Health Assessment (item 715), refugee health assessments (items 701/703/705), and antenatal booking bloods.

Serology interpretation

Understanding the CHB serological panel is essential:

ResultHBsAgAnti-HBcAnti-HBsInterpretation
Current infection++Active HBV; confirm chronic (>6 months)
Past infection (resolved)++Immunity from past infection
Vaccinated immune+Immunity from vaccination
SusceptibleNo immunity; offer vaccination
Chronic hepatitis B++>6 months HBsAg positive = chronic

In established CHB, also check: HBeAg and anti-HBe (replication markers; HBeAg seroconversion is a treatment landmark), HBV DNA viral load (quantitative PCR — guides treatment decisions), and anti-HDV (hepatitis D virus — all CHB patients should be tested at least once, as delta superinfection accelerates fibrosis and changes management).

Natural history — five-phase model

Modern classification (EASL 2017) uses five phases:

  1. HBeAg-positive chronic infection (immune-tolerant) — high viral load, normal ALT, minimal inflammation; common in vertically infected young adults
  2. HBeAg-positive chronic hepatitis (immune-active) — high viral load, elevated ALT, active liver inflammation; this is the phase most likely to require treatment
  3. HBeAg-negative chronic infection (inactive carrier) — low viral load (<2,000 IU/mL), normal ALT, minimal fibrosis; low but non-zero risk of HCC
  4. HBeAg-negative chronic hepatitis (immune-escape) — moderate-to-high viral load (>2,000 IU/mL), fluctuating ALT, anti-HBe positive; ongoing liver injury; requires treatment consideration
  5. HBsAg loss / functional cure — spontaneous in approximately 1–2% per year; protective; treatment may be stopped after confirmed sustained loss

HCC can develop in any phase, particularly in at-risk groups, which is why surveillance is not limited to those with cirrhosis.

Workup

Initial assessment:

  • Liver function tests (ALT, AST, GGT, ALP, bilirubin, albumin, INR)
  • Full blood count (platelets — low in advanced fibrosis)
  • Renal function and eGFR (baseline before tenofovir)
  • HBV DNA viral load
  • HBeAg / anti-HBe
  • Anti-HDV (at least once in every CHB patient)
  • Co-infection screen: HCV, HIV
  • Alpha-fetoprotein (AFP) — baseline for HCC surveillance
  • Liver ultrasound — baseline and 6-monthly in at-risk groups for HCC surveillance
  • FibroScan (transient elastography) — non-invasive fibrosis staging; largely replaces biopsy

Non-invasive fibrosis scores: APRI and FIB-4 can stratify fibrosis risk using standard bloods and are useful when FibroScan is not immediately available.

Treatment indications

Per synthesised ASHM, GESA, EASL, and AASLD guidance — treat when:

  1. HBeAg-positive immune-active hepatitis: HBV DNA >20,000 IU/mL + elevated ALT + significant fibrosis
  2. HBeAg-negative immune-escape hepatitis: HBV DNA >2,000 IU/mL + elevated ALT + significant fibrosis
  3. Cirrhosis (compensated or decompensated): any detectable HBV DNA
  4. Pregnancy: HBV DNA >200,000 IU/mL — tenofovir from 28–30 weeks to reduce vertical transmission risk
  5. Immunosuppression or chemotherapy: prophylactic antivirals to prevent HBV reactivation (HBsAg-positive always; anti-HBc-positive considered for high-risk regimens including rituximab, anti-CD20, and allogeneic stem cell transplant)
  6. HCC: independent of viral parameters
  7. Extrahepatic manifestations: polyarteritis nodosa, membranous glomerulonephritis

Don’t treat (monitor):

  • HBeAg-positive chronic infection without significant fibrosis (immune-tolerant)
  • HBeAg-negative inactive carrier with persistent HBV DNA <2,000 IU/mL and normal ALT

First-line antivirals

Per eTG Chronic hepatitis B and PBS Section 100 authority criteria:

AgentDoseNotes
Tenofovir disoproxil fumarate (TDF, Viread)300 mg dailyFirst-line; monitor eGFR and phosphate (Fanconi syndrome risk)
Tenofovir alafenamide (TAF, Vemlidy)25 mg dailyPreferred if eGFR <60, osteoporosis, or elderly; less renal/bone toxicity
Entecavir (Baraclude)0.5 mg daily (1 mg if lamivudine-resistant)Take on empty stomach; caution in decompensated cirrhosis

Avoid lamivudine as first-line — high resistance rate (approximately 70% by five years). Pegylated interferon is reserved for selected younger patients (HBeAg-positive, low viral load, favourable genotype) who want a finite-course option; the many side effects and modest HBsAg-loss rate limit its use.

Treatment is typically lifelong. Discontinuation is considered only after confirmed sustained HBsAg loss under specialist guidance.

B. Evidence appraisal

Antiviral efficacy

Large randomised trials demonstrate that TDF and entecavir each suppress HBV DNA to undetectable levels in over 95% of treated patients by week 48, with minimal resistance emergence at five years (unlike lamivudine). HBeAg seroconversion — a favourable treatment landmark — occurs in 20–30% of HBeAg-positive patients within two years of treatment. Long-term antiviral use reduces progression to cirrhosis, hepatic decompensation, and HCC compared to untreated historical cohorts.

HCC surveillance evidence

Surveillance with 6-monthly liver ultrasound plus AFP in at-risk CHB patients detects HCC at an earlier, potentially resectable stage compared to incidental detection. HCC in CHB without cirrhosis is well-documented — the recognition that cirrhosis is not a prerequisite for HCC in CHB drove the current age- and ancestry-based surveillance criteria.

Vertical transmission prevention

The combination of HBIG within 12 hours of birth plus the complete vaccination schedule reduces mother-to-child HBV transmission to under 5% even in HBeAg-positive mothers. When maternal HBV DNA exceeds 200,000 IU/mL, adding tenofovir from 28–30 weeks of gestation reduces transmission further to under 1%. This strategy is now standard of care in Australian obstetric practice per Australian Immunisation Handbook and antenatal guidelines.

Reactivation prophylaxis

HBV reactivation in HBsAg-positive individuals receiving immunosuppression or cytotoxic chemotherapy can be severe and sometimes fatal. Evidence from multiple cohort studies and meta-analyses supports prophylactic antiviral therapy throughout immunosuppressive treatment and for several months after completion. Rituximab and other anti-CD20 agents carry particularly high reactivation risk even in patients with resolved infection (HBsAg-negative, anti-HBc-positive).

Vaccination

Universal infant vaccination (birth dose plus 2/4/6 months combined hexavalent vaccine) has substantially reduced CHB prevalence in birth cohorts since its introduction. Adult vaccination with the standard 3-dose schedule (0, 1, 6 months) achieves seroprotection in over 95% of immunocompetent adults. Heplisav-B (adjuvanted 2-dose schedule, 1 month apart) achieves faster and often superior response, particularly useful for non-responders or those needing rapid protection.

C. HCC surveillance in Australian general practice

HCC surveillance is a GP responsibility for many CHB patients, especially those not currently requiring antiviral treatment. The criteria for 6-monthly ultrasound plus AFP:

  • All patients with established cirrhosis (any cause, including CHB)
  • Asian-ancestry men with CHB aged over 40
  • Asian-ancestry women with CHB aged over 50
  • Aboriginal and Torres Strait Islander Australians with CHB aged over 50 (some guidelines suggest 40)
  • African-ancestry individuals with CHB at any adult age
  • Any CHB patient with a first-degree family history of HCC
  • Persistent or fluctuating elevated ALT with HBV DNA >2,000 IU/mL

An imaging reminder or recall system is essential. A normal ultrasound and AFP does not rule out interval HCC development — the 6-month interval reflects the tumour doubling time of HCC and should not be extended routinely. Any detected nodule or AFP rise warrants urgent hepatology or multidisciplinary liver tumour board assessment.

Per MBS Online, liver ultrasound is funded under items 55028/55036, and AFP under pathology. GPs can request both.

D. Australian operations

Section 100 community prescribing

Australia has a distinctive model where accredited GPs — after ASHM-led training and assessment — can prescribe HBV antivirals under the PBS Section 100 Highly Specialised Drugs Community Access program. This model:

  • Enables long-term management of stable CHB patients in general practice without requiring every prescription visit to a hepatologist
  • Reduces access barriers, particularly in regional and remote areas
  • Requires an initial specialist consultation for treatment initiation in most cases
  • Requires ongoing liaison with a specialist as needed

ASHM provides the Section 100 prescriber training, the HBV Clinical Decision-Making tool (hepatitisb.ashm.org.au), and practice support resources. This is a genuine and important GP role worth pursuing for practices with CHB patient cohorts.

MBS billing

ItemUse
23/36/44Standard GP consultations
132/133Complex chronic disease management (hepatology)
715ATSI health assessment (includes CHB screening)
701/703/705Refugee health assessments
55028/55036Abdominal / liver ultrasound (HCC surveillance)
73807LFT and serology bundle
73881Quantitative HBV DNA (Authority)
965/967GP Chronic Disease Management Plan (enables allied health, dietitian, mental health)

Notification

Hepatitis B is a notifiable disease in all Australian jurisdictions. The laboratory typically submits notification automatically, but clinical notification may also be required in some states. Check your state or territory public health unit requirements.

Key Australian resources

  • ASHM — Section 100 prescriber training, HBV clinical decision-making tool, clinical guidelines
  • GESA — Australia and New Zealand CHB guidelines, liver disease resources
  • Hepatitis Australia — patient organisation; community navigation, support, stigma resources
  • State hepatitis organisations — Hepatitis NSW, Hepatitis Victoria, etc. — community language resources

Refugee and migrant health

CHB is one of the most common chronic conditions detected in newly arrived refugees and migrants. Refugee health assessments (MBS items 701/703/705) include CHB serology screening as standard. For patients diagnosed with CHB through refugee health pathways, free antiviral therapy is available via Section 100 for eligible patients, removing cost as a barrier.

E. Special populations

Pregnant women: all pregnant women are screened for HBsAg at booking bloods. HBsAg-positive mothers need HBV DNA tested at 26–28 weeks. If DNA exceeds 200,000 IU/mL, begin tenofovir disoproxil fumarate at 28–30 weeks and continue to delivery. Breastfeeding is safe, including on tenofovir. Infants of HBsAg-positive mothers receive HBIG within 12 hours of birth plus standard vaccination; post-vaccination serology (HBsAg and anti-HBs) at 9–12 months confirms protection.

Immunosuppressed patients and those receiving chemotherapy: never commence cytotoxic chemotherapy, biologic therapy (particularly rituximab), or transplant immunosuppression in an HBsAg-positive patient without antiviral prophylaxis. Entecavir or TDF cover should continue throughout treatment and typically for 12 months after completion (longer after anti-CD20 agents). Anti-HBc-positive patients (resolved infection) who receive high-risk regimens also need monitoring and possible prophylaxis under specialist guidance.

Aboriginal and Torres Strait Islander Australians: higher CHB prevalence and higher HCC burden, partly from delayed diagnosis and later presentation. The 715 health assessment is the key GP gateway for CHB detection, surveillance, and linkage to treatment. Culturally safe care — including involvement of Aboriginal Health Workers and community-controlled health services — improves engagement and outcomes. NPS MedicineWise provides translated and culturally adapted CHB resources.

Children: most children with CHB in Australia acquired it vertically. They are typically in the immune-tolerant phase and do not require treatment, but need regular monitoring. Paediatric hepatology should be involved in management decisions for children.

People who inject drugs: harm reduction services (needle and syringe programs), hepatitis B vaccination, and linking to Section 100 prescribers are the evidence-based levers. Stigma reduction in the clinical encounter is essential to engagement.

When to escalate

  • Treatment initiation required (immune-active or cirrhotic CHB) — specialist hepatology or GP with Section 100 accreditation
  • Decompensated cirrhosis (ascites, encephalopathy, variceal bleeding, jaundice) — urgent hepatology and liver transplant assessment
  • HCC suspected — nodule on surveillance ultrasound or AFP rise — urgent hepatology or liver tumour board
  • Pregnancy with CHB — shared care with obstetrics and hepatology; tenofovir initiation if viral load >200,000 IU/mL
  • Pre-immunosuppression assessment — always check and manage HBsAg/anti-HBc status before commencing rituximab, allogeneic transplant, or other high-risk regimens
  • HDV co-infection confirmed — specialist hepatology; bulevirtide is an emerging treatment option
  • Paediatric CHB — paediatric gastroenterology / hepatology

What this article is and is not

This is general health information drawn from ASHM CHB guidelines, GESA guidelines, eTG, the Australian Immunisation Handbook, and consensus from AASLD, EASL, and WHO. It is not personal medical advice and does not create a doctor–patient relationship. Treatment decisions for CHB are complex and should be made with a GP holding Section 100 prescribing accreditation or a hepatologist or infectious diseases specialist.

For patient-facing information: Hepatitis Australia, HealthDirect — Hepatitis B, NPS MedicineWise.


Sources cited

  1. ASHM — Hepatitis B management in general practice (3rd edition)
  2. GESA — Australia and New Zealand Chronic Hepatitis B Guidelines
  3. Therapeutic Guidelines (eTG) — Chronic hepatitis B
  4. Australian Immunisation Handbook — Hepatitis B
  5. AASLD 2018 — Hepatitis B guidance (Terrault et al.)
  6. EASL 2017 — Clinical practice guidelines on HBV management
  7. WHO — Hepatitis B guidelines 2024
  8. Hepatitis Australia
  9. PBS Schedule — Section 100 community access antivirals
  10. MBS Online — hepatology and surveillance items
  11. HealthDirect — Hepatitis B
  12. NPS MedicineWise

Frequently asked questions

  • How do I find out if I have hepatitis B?

    A blood test for hepatitis B surface antigen (HBsAg) detects current infection; a negative result with positive antibody (anti-HBs) indicates immunity from vaccination or past infection. People at higher risk should ask their GP for hepatitis B serology testing: migrants from Asia, sub-Saharan Africa, or the Pacific Islands; Aboriginal and Torres Strait Islander people; people who inject drugs; sex workers; men who have sex with men; and those with a family member living with CHB. Many Medicare-funded health assessments, including the Aboriginal and Torres Strait Islander Health Assessment (item 715), include hepatitis B screening.

  • What are the phases of chronic hepatitis B?

    Chronic hepatitis B passes through several phases depending on the interaction between the virus and the immune system. In the immune-tolerant phase the viral load is high but the liver is relatively undamaged — common after infection in infancy. In the immune-active phase the immune system responds more vigorously, liver inflammation rises, and this is when treatment is typically considered. The inactive carrier phase sees the virus suppressed with minimal liver activity. A fourth phase of HBeAg-negative active hepatitis involves fluctuating viral activity despite loss of HBeAg. A small proportion achieve HBsAg loss, sometimes called functional cure. Lifelong monitoring is standard for all phases.

  • When is antiviral treatment needed?

    Treatment decisions are made jointly with a specialist or a GP holding Section 100 prescribing accreditation. Treatment is generally indicated when: the liver enzyme ALT is elevated, HBV DNA exceeds defined thresholds (broadly over 2,000 IU/mL in HBeAg-negative disease or over 20,000 IU/mL in HBeAg-positive disease), and significant liver fibrosis is present on non-invasive assessment. All patients with cirrhosis should be on antivirals regardless of viral load. Antiviral therapy is also used in pregnancy when viral load exceeds 200,000 IU/mL to reduce the risk of passing the virus to the baby.

  • Can I pass hepatitis B to my family or partner?

    Yes — hepatitis B transmits through sexual contact, sharing of razors or toothbrushes, and from mother to child at or around birth. The good news is that vaccination is highly effective. All household contacts and sexual partners should have their immunity checked and receive vaccination if not immune. Infants born to mothers with hepatitis B receive hepatitis B immune globulin (HBIG) within twelve hours of birth plus the standard vaccination schedule — this combination prevents vertical transmission in almost all cases when started promptly.

  • Do I need liver cancer surveillance?

    Yes, if you fall into higher-risk groups. People with chronic hepatitis B who need six-monthly liver ultrasound and alpha-fetoprotein (AFP) testing for hepatocellular carcinoma surveillance include: Asian-ancestry men over 40, Asian-ancestry women over 50, Aboriginal and Torres Strait Islander Australians over 50, all people with cirrhosis, people from African backgrounds at any adult age, and anyone with a first-degree family history of liver cancer. Importantly, hepatocellular carcinoma can develop in chronic hepatitis B even without cirrhosis — surveillance is based on age, ancestry, and family history, not cirrhosis status alone.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.