Decision support only — urgent hepatology/transplant discussion for liver failure or decompensation; notify new acute/chronic infection as required; verify doses, renal adjustment, pregnancy care and PBS eligibility locally.
1 Start with the right test, then stage the person
HBV is dynamic. One ALT and one viral load do not define a lifelong “phase”, and a normal ALT does not prove harmless infection. First establish the serological pattern; then pair HBV DNA with repeated ALT, fibrosis, age, comorbidity and cancer risk.
Risk, exposure, abnormal liver tests, pregnancy, immunosuppression — or a positive HBsAgOrder the triple panel: HBsAg + total anti-HBc + anti-HBs. On the Australian request slip, “? chronic hepatitis B” supports MBS testing of all three.
Interpret the pattern; if HBsAg positive, do not wait six months to assess severity
CURRENT INFECTION → BASELINE STAGE NOW
ACUTE HBV OR A CHRONIC FLARE?IgM anti-HBc supports acute infection when the titre and clinical picture fit, but it can also be positive during a chronic flare. Do not diagnose “acute HBV” from IgM alone. Prior results, exposure timing, HBsAg persistence and longitudinal DNA/ALT settle it. ASHM
1 · DEFINE SEVERITY
Symptoms + examination: jaundice, encephalopathy, bleeding; ascites, oedema, splenomegaly; pregnancy; immunosuppression; extrahepatic vasculitis or glomerulonephritis.
Bloods: ALT/AST, bilirubin, ALP/GGT, albumin, INR, FBC/platelets, creatinine/eGFR; glucose if acutely unwell.
Urgent hepatology/transplant centre: encephalopathy, worsening INR/synthetic failure, rapidly rising bilirubin, hypoglycaemia, decompensated cirrhosis or severe flare during/after immunosuppression.
2 · DEFINE THE VIRUS
HBV: HBeAg + anti-HBe, quantitative HBV DNA. Repeat ALT/DNA because phase assignment is longitudinal.
Co-infection: anti-HCV, HIV Ag/Ab and anti-HDV in every HBsAg-positive person; if anti-HDV positive, obtain HDV RNA and refer. Check HAV immunity. GESA/WHO
Australian ALT ULN: use 19 U/L women and 30 U/L men for HBV phase/treatment assessment, not an unusually high local laboratory ceiling. GESA 2022
3 · DEFINE THE LIVER + RISK
Fibrosis: transient elastography where available plus APRI/FIB-4; interpret stiffness cautiously during an ALT flare. Biopsy only when it will resolve a treatment or diagnostic question.
Imaging: baseline liver ultrasound; look for cirrhosis/portal hypertension and decide whether formal six-monthly HCC surveillance starts now.
Risk modifiers: age, country of birth/ethnicity, Aboriginal or Torres Strait Islander status, family HCC/cirrhosis, alcohol, MASLD/diabetes, immunosuppression and prior antiviral exposure.
2 Serology: say exactly what the pattern proves
| HBsAg | Total anti-HBc | Anti-HBs | Interpretation | Next move |
|---|
| − | − | − | Susceptible, unless very early incubation. | Vaccinate if indicated; use exposure-specific PEP if relevant. |
| − | − | + | Immune after vaccination. | No infection. Document anti-HBs ≥10 mIU/mL after a completed course when post-vaccination testing is indicated. |
| − | + | + | Resolved infection. HBV can persist as cccDNA. | No routine antiviral treatment, but record it: reactivation remains possible with immunosuppression. |
| + | + | − | Current infection. Chronic if HBsAg persists ≥6 months; acute is a clinicopathological diagnosis. | IgM anti-HBc if acute suspected; stage immediately with DNA, ALT, fibrosis and severity tests. |
| − | + | − | Isolated core antibody: often remote resolved infection; also false positive, window period, waned anti-HBs or occult HBV. | Repeat panel. Check IgM if acute exposure; obtain HBV DNA before high-risk immunosuppression or if occult infection matters. |
“Immune control” is not viral eradication
HBsAg loss is the best routinely measurable endpoint, but intrahepatic cccDNA can persist after resolved infection. That is why an old anti-HBc result matters before rituximab, stem-cell transplantation or other substantial immunosuppression. ASHM · EASL 2025
3 Classify chronic HBV — and recognise the grey zone
Use the modern phase names; avoid “healthy carrier”. Thresholds help organise care, but repeat results and look for fibrosis. A patient can move between phases, especially around HBeAg seroconversion, pregnancy and immunosuppression.
| Working phase | Typical pattern | Registrar action | Treatment implication |
|---|
HBeAg-positive chronic infection
old: immune tolerant | HBeAg+, usually very high DNA, repeatedly normal ALT; no significant fibrosis. | ALT q6 months; DNA annually; HBeAg/anti-HBe q6–12 months; fibrosis reassessment. Scrutinise age >40, family HCC, fibrosis and comorbidity. | Australian GESA: not routine if genuinely low-risk. WHO 2024/AASLD 2025 favour treatment with significant fibrosis or important risk modifiers; discuss rather than ignoring. |
| HBeAg-positive chronic hepatitis | HBeAg+, HBV DNA >20,000 IU/mL with persistent ALT elevation and/or significant inflammation/fibrosis. | Treat after staging; urgently if cirrhosis or decompensation. GESA 2022 | Meets the main Australian clinical threshold. Non-cirrhotic PBS eligibility also needs documented chronic liver injury. |
HBeAg-negative chronic infection
old: inactive carrier | HBeAg−/anti-HBe+, DNA <2,000 IU/mL, repeatedly normal ALT, no significant fibrosis. | ALT q6–12 months; DNA and fibrosis approximately annually. Investigate MASLD, alcohol, HCV/HDV and other causes if ALT rises. | Usually monitor, not treat. Continue HCC surveillance if independently indicated. |
| HBeAg-negative chronic hepatitis | HBeAg−, DNA >2,000 IU/mL with persistent ALT elevation and/or significant inflammation/fibrosis. | Treat after staging. HBeAg negativity does not mean low-risk infection. GESA 2022 | Meets the main Australian clinical threshold; confirm the live PBS injury requirement. |
| Indeterminate / grey zone | DNA and ALT do not fall neatly into the rows above, or fluctuate; age/fibrosis/risk points in a different direction from the labs. | Repeat ALT/DNA, exclude another liver disease, obtain good fibrosis assessment and discuss with hepatology. | Do not use “monitor” as an indefinite holding pattern. WHO/EASL/AASLD have moved toward risk-based treatment beyond old phase boxes. |
4 Treatment algorithm: clinical indication first, PBS second
Treat now / urgent specialist management
- CIRRHOSISCompensated or decompensated cirrhosis with any detectable HBV DNA. Do not wait for ALT to rise. GESA · PBS
- LIVER FAILURESevere/protracted acute HBV, acute liver failure or acute-on-chronic failure: high-barrier NA plus urgent hepatology/transplant input. Uncomplicated acute HBV is usually supportive care.
- REACTIVATIONHBsAg-positive person starting material immunosuppression; or high-risk resolved infection. Start prophylaxis before or with immunosuppression.
- SPECIALClinically significant HBV extrahepatic disease; HBV/HIV coinfection within suppressive ART; high-viraemia pregnancy prophylaxis.
Non-cirrhotic chronic HBV
- HBeAg+Treat when DNA >20,000 IU/mL plus persistent ALT elevation or significant inflammation/fibrosis. GESA 2022
- HBeAg−Treat when DNA >2,000 IU/mL plus persistent ALT elevation or significant inflammation/fibrosis. GESA 2022
- ≥F2WHO 2024 recommends treatment for significant fibrosis, regardless of ALT/DNA; EASL/AASLD also broaden treatment according to fibrosis, age and HCC risk.
- RISKRefer even if the classic box is not met when there is family HCC/cirrhosis, HDV/HCV/HIV, immunosuppression, diabetes/MASLD, extrahepatic disease or age-related concern.
PBS eligibility is narrower than modern clinical eligibility
August 2026 General Schedule: non-cirrhotic entecavir/TDF requires HBV DNA >20,000 IU/mL if HBeAg-positive or >2,000 IU/mL if HBeAg-negative, plus evidence of chronic liver injury through confirmed elevated ALT or biopsy. Cirrhosis requires detectable DNA. TDF also has a streamlined pregnancy restriction for DNA >200,000 IU/mL in the third trimester, continuing for prevention of reactivation up to 12 weeks postpartum. A strong clinical reason to treat does not manufacture a PBS code; check the live restriction or arrange specialist access. PBS AUG 2026
5 Choose the antiviral, then monitor what it can harm
Current nucleos(t)ide analogues are excellent suppression drugs and poor cure drugs. The practical targets are undetectable HBV DNA, biochemical control and prevention of cirrhosis, liver failure and HCC. Functional cure means sustained HBsAg loss with undetectable HBV DNA after treatment, with or without anti-HBs; it remains uncommon. A suppressed viral load is therefore not permission to stop treatment or cancer surveillance. WHO 2024 · EASL 2025
| Option | Usual adult regimen | Best fit | Watch / avoid | Australian access |
|---|
| Tenofovir DF (TDF) | 300 mg PO daily; renal interval adjustment when required. | Preferred in pregnancy; active after lamivudine resistance; potent, high resistance barrier. GESA/ASHM | Baseline and serial creatinine/eGFR and phosphate; consider urinalysis. Bone/renal toxicity matters, especially CKD, osteoporosis or interacting nephrotoxins. | PBS for eligible chronic HBV and high-viraemia pregnancy under separate restrictions. |
| Entecavir (ETV) | 0.5 mg PO daily treatment-naïve; 1 mg daily if lamivudine-resistant/refractory or decompensated. Take fasting; adjust for renal function. | Potent first-line option when pregnancy is not relevant and there is no lamivudine resistance. | Test for HIV before HBV monotherapy. Do not use as lone HIV treatment; resistance barrier falls after lamivudine resistance. | PBS restrictions differ for 0.5 mg versus 1 mg; verify the exact code. |
| Tenofovir AF (TAF) | 25 mg PO daily with food. | Society-endorsed high-barrier option with less renal/bone biomarker change than TDF; useful when renal/bone risk dominates. | Still assess renal disease and interactions. TDF has the longer pregnancy safety record in Australian guidance. | Not PBS-listed as HBV monotherapy in the August 2026 General Schedule. Do not confuse HIV combination listings with HBV subsidy. |
| Peg-IFN alfa-2a | 180 micrograms SC weekly × 48 weeks. | Selected compensated, treatment-naïve patients seeking a finite course and with favourable virological features; hepatology-led. | Contraindicated in decompensated cirrhosis and pregnancy; major psychiatric, autoimmune, cytopenic and systemic toxicity. | Specialist selection; verify indication and subsidy before prescribing. |
On NA treatment
ALT, HBV DNA, adherence and drug toxicity about every 3 months in year 1, then generally every 6 months once stable. Follow HBeAg/anti-HBe if initially positive; HBsAg/anti-HBs annually once DNA is suppressed. Continue HCC surveillance independently. ASHM
Virological breakthrough
Confirm the result and ask about missed doses, pharmacy access and interactions before declaring resistance. A tenfold DNA rise from nadir is meaningful; seek specialist resistance testing/therapy advice rather than adding a low-barrier drug.
Stopping is a clinical procedure
Never stop in cirrhosis. For HBeAg-negative disease, AASLD 2025 favours continuing until HBsAg loss. Any finite-NA strategy needs specialist selection, explicit flare thresholds and close post-stop DNA/ALT monitoring. Accidental cessation can decompensate.
6 Pregnancy, immunosuppression and coinfection
Pregnancy + newborn
- SCREENHBsAg in every pregnancy. If positive: DNA early and again around 26–28 weeks, ALT, HBeAg, fibrosis/clinical stage; link to specialist care.
- MOTHERIf DNA >200,000 IU/mL, offer TDF 300 mg daily from week 28 (PBS: third trimester), generally through 2–12 weeks postpartum. Treat maternal disease on its own merits. GESA/PBS
- INFANTHBIG 100 IU IM + monovalent HBV vaccine 0.5 mL IM immediately after birth at separate sites; ideally within 4 h and certainly within 12 h. Then vaccine at 2, 4 and 6 months.
- CHECKHBsAg + anti-HBs at 9–12 months and at least 3 months after the final vaccine. Breastfeeding is acceptable. Monitor maternal ALT after delivery; flares are common.
Immunosuppression
- BEFOREHBsAg + anti-HBc + anti-HBs before chemotherapy, biologics, high-dose/prolonged steroids, transplantation or other substantial immune suppression.
- HBsAg+Cancer chemotherapy or moderate/high-risk immunosuppression: ETV or TDF before/at treatment, regardless of baseline DNA. For low-risk non-malignant therapy, GESA permits structured 3-monthly ALT and 6-monthly DNA monitoring instead.
- RESOLVEDHBsAg−/anti-HBc+: prophylaxis for anti-CD20/B-cell depletion and stem-cell transplantation; for lesser risk, choose prophylaxis or reliable HBV DNA/ALT/HBsAg surveillance.
- DURATIONAustralian guidance: continue ≥12 months after most regimens and ≥24 months after B-cell-depleting therapy, with monitoring after cessation. ASHM
HIV, HDV and HCV
- HIVUse suppressive ART containing two HBV-active agents, usually TDF/TAF + FTC/3TC. Do not give entecavir as unsuppressed HIV monotherapy, and do not stop HBV-active ART casually.
- HDVTest all HBsAg-positive people with anti-HDV; confirm active infection with HDV RNA. NAs suppress HBV but do not treat HDV itself. Refer early. GESA/WHO
- HCVHBsAg/anti-HBc/anti-HBs before DAA therapy. HBsAg-positive people need HBV treatment or structured DNA/ALT monitoring because reactivation can occur.
7 HCC surveillance and routine follow-up
| Start ultrasound every 6 months ± AFP | Australian risk group |
|---|
| Any cirrhosis | Regardless of treatment or viral suppression. |
| Asian-Pacific ancestry | Men from age 40; women from age 50. |
| Sub-Saharan African origin | From age 20. |
| Aboriginal or Torres Strait Islander | From age 50; consider from age 40 with additional risk factors. |
| First-degree family history of HCC | From age 40; consider 10 years before the earliest family diagnosis. |
HBV can cause HCC without cirrhosis
Viral DNA integration and persistent viral protein expression contribute direct oncogenic pressure alongside chronic inflammation and fibrosis. That is why Australian surveillance follows population and family risk as well as cirrhosis. Viral suppression lowers risk but does not cancel it: continue surveillance when the person met criteria before treatment, including after HBsAg loss when a major risk indication remains. If ultrasound quality is repeatedly poor, discuss an alternative imaging strategy rather than pretending a limited scan was surveillance. ASHM · EASL 2025
At each longitudinal review
- ACTIVITYALT trend, HBV DNA and HBeAg status where relevant; ask about adherence and new medicines.
- STAGEPlatelets/synthetic function, fibrosis trajectory and features of decompensation. A normal ALT does not overrule cirrhosis.
- TOXICITYRenal function/phosphate for TDF; renal dose adjustment for ETV; bone risk where clinically relevant.
- CANCERIs six-monthly HCC surveillance due? Document the next date rather than “continue surveillance”.
- COFACTORSAlcohol, weight/MASLD, diabetes, smoking; HAV immunity/vaccination; HIV/HCV/HDV status if not complete or if new risk.
- CONTACTSHousehold/sexual contacts tested and vaccinated; pregnancy plans; occupational or exposure advice; disclosure handled without stigma.
8 Prevention, notification and post-exposure action
Practical prevention
- CONTACTSOffer triple-panel testing and vaccination to sexual, household and household-like contacts. Use condoms until immunity is documented where transmission risk persists.
- VACCINERoutine infant schedule: birth, 2, 4 and 6 months. Most adult risk groups: 0, 1 and 6 months; use the product/age-specific Australian schedule.
- ANTI-HBsCheck 4–8 weeks after the course when occupational risk, immunocompromise, dialysis/poor response, significant liver disease or close-contact status makes proof of response important. Protective response: ≥10 mIU/mL.
- NOTIFYAcute HBV and newly identified chronic HBV are notifiable in all Australian jurisdictions. Follow local public-health processes.
- NORMAL LIFENo sharing razors/toothbrushes or injecting equipment; cover blood spills. HBV is not spread by food, hugging or ordinary workplace contact.
| Non-immune exposure to HBsAg+ / unknown source | HBIG | Vaccine |
|---|
| Percutaneous, ocular or mucosal | 400 IU IM (100 IU if <30 kg) once, within 72 h. | Start ASAP, within 7 days; subsequent doses at 1 and 6 months. |
| Sexual exposure | 400 IU IM (100 IU if <30 kg) preferably within 72 h; can be given up to 14 days. | Start ASAP, within 14 days; subsequent doses at 1 and 6 months. |
| Previously vaccinated + documented responder | None. | No PEP if anti-HBs ≥10 mIU/mL was documented at any time after vaccination. |
Collect source and exposed-person bloods promptly, but do not delay indicated HBIG/vaccine while waiting. Use the current Australian Immunisation Handbook table for non-response, unknown response, neonatal exposure and product-specific dosing.
Primary source —
GESA Australian Consensus Recommendations for CHB (2022) and the current
ASHM B Positive, 4th ed., including chapters on
testing,
assessment,
treatment,
pregnancy/children and
complex situations. Subsidy checked against the
PBS General Schedule, August 2026, Vol 2. Vaccination/PEP:
Australian Immunisation Handbook: hepatitis B (updated Jan 2026). International cross-check:
WHO CHB guideline 2024;
EASL HBV CPG 2025;
AASLD/IDSA HBV treatment guideline 2025 (Hepatology 2026).
Key trials — REVEAL-HBV cohorts:
Chen et al., JAMA 2006 (HBV DNA gradient and HCC) and
Iloeje et al., Gastroenterology 2006 (DNA and cirrhosis);
Marcellin et al., NEJM 2008 (TDF vs adefovir);
Chang et al., Hepatology 2010 (long-term entecavir histology);
Pan et al., NEJM 2016 and
Jourdain et al., NEJM 2018 (maternal TDF in high-quality neonatal immunoprophylaxis settings).
Caveats — GESA/ASHM 2022 remains the Australian practice backbone, while WHO 2024, EASL 2025 and AASLD/IDSA 2025 broaden or reframe treatment for fibrosis, age and cancer risk. This sheet separates those clinical recommendations from current PBS wording. PBS restrictions and product availability can change; check live. HCC thresholds are population-risk tools, not guarantees; HBV-related HCC can occur without cirrhosis through direct and indirect carcinogenic pathways (see
HBV integration review, 2025). Ultrasound performance falls with obesity/nodular livers. Antiviral suppression reduces cirrhosis/HCC risk but is not sterilising cure and usually requires long-term therapy.