📋 Key Information Summary
- Hepatitis B (HBV) and hepatitis C (HCV) are leading causes of cirrhosis, hepatocellular carcinoma (HCC), and liver-related mortality in Australia — most infected individuals remain undiagnosed.
- HBV screening is recommended for all people born in endemic regions (Asia, Pacific Islands, sub-Saharan Africa, Eastern Europe), Aboriginal and Torres Strait Islander peoples, people who inject drugs (PWID), men who have sex with men (MSM), prisoners, HIV/HCV co-infected individuals, dialysis patients, pregnant women, and household/sexual contacts of known carriers.
- HCV screening is recommended for all PWID (test at least annually), recipients of blood products before February 1990, people on haemodialysis, people with HIV, prisoners, children born to HCV-positive mothers, and anyone with unexplained elevated ALT.
- Initial HBV evaluation uses a serological panel: HBsAg, anti-HBs, anti-HBc (± HBeAg/anti-HBe, HBV DNA). HCV screening uses anti-HCV antibody with reflex HCV PCR (RNA) to confirm active infection.
- All patients with confirmed HBV or HCV infection require LFTs, full blood count, coagulation studies, and fibrosis assessment (APRI score, FIB-4, or transient elastography).
- HCV is now curable in >95% of cases with 8–12 weeks of direct-acting antivirals (DAAs) — treatment is PBS-listed and can be initiated by GPs with s100 authority.
- HBV is rarely cured but can be effectively suppressed with long-term nucleos(t)ide analogues (tenofovir or entecavir); treatment decisions require specialist input.
- All newly diagnosed HBV/HCV patients must be linked to a hepatologist, gastroenterologist, or infectious disease specialist for antiviral eligibility assessment and long-term HCC surveillance planning.
- Vaccinate all susceptible household and sexual contacts of HBV carriers against hepatitis B (HBV vaccine is funded under the NIP).
- No HCV vaccine exists — harm-reduction counselling (needle exchange, safe injecting practices) is essential for PWID to prevent reinfection and onward transmission.
- Aboriginal and Torres Strait Islander peoples have significantly higher rates of HBV and HCV — proactive, culturally safe screening in primary care and correctional settings is critical to closing the gap.
- HBV-positive patients require lifelong HCC surveillance with 6-monthly abdominal ultrasound ± AFP, even if not on antiviral therapy.
Introduction & Australian Epidemiology
Hepatitis B virus (HBV) and hepatitis C virus (HCV) are the most common chronic blood-borne viral infections in Australia. Together they account for the majority of chronic liver disease, cirrhosis, and hepatocellular carcinoma (HCC) nationally. Despite the availability of an effective HBV vaccine and curative HCV therapies, both infections remain significantly underdiagnosed and undertreated in the Australian population.
Primary care plays a central role in hepatitis elimination. The Australian Government has committed to the WHO targets of eliminating viral hepatitis as a public health threat by 2030, requiring a substantial scale-up of testing, linkage to care, and treatment in general practice settings.
Hepatitis B in Australia
- An estimated 223,000–300,000 people are living with chronic HBV in Australia (prevalence ~1%).
- Approximately 38–50% remain undiagnosed.
- The most affected populations include people born in endemic countries (China, Vietnam, Philippines, Korea, sub-Saharan Africa, Pacific Islands), Aboriginal and Torres Strait Islander peoples, and people with a history of injecting drug use.
- Mother-to-child transmission (MTCT) remains the most important route in endemic populations; sexual and percutaneous transmission predominate in Australian-born populations.
- HBV-related HCC incidence is increasing and is now the fastest-rising cause of cancer death in Australian males.
- The NIP funds HBV vaccination for all infants (since 2000), catch-up for adolescents, and for high-risk adults (Aboriginal and Torres Strait Islander peoples from 15 years, PWID, MSM, household contacts, dialysis patients, healthcare workers).
Hepatitis C in Australia
- An estimated 115,000–175,000 people are living with chronic HCV; approximately 20% remain undiagnosed.
- Over 90% of new HCV infections in Australia are acquired through sharing of injecting equipment among PWID.
- Since the introduction of PBS-funded DAAs in March 2016, over 100,000 Australians have been treated and cured, but treatment uptake has plateaued since 2020.
- Reinfection rates among PWID are 2–8% per year, underscoring the need for ongoing harm-reduction services post-cure.
- HCV-related cirrhosis and HCC remain significant causes of liver transplant and liver-related mortality.
Under-diagnosis is the primary barrier to elimination. The majority of Australians with chronic HBV and a substantial proportion with HCV are unaware of their infection. GPs should adopt an opt-out testing approach for at-risk populations rather than waiting for clinical symptoms.
Screening Indications
Screening for HBV and HCV should be offered proactively to individuals meeting defined risk criteria. Testing should be framed as routine and non-stigmatizing — a standard part of preventive healthcare rather than an indicator of assumed behaviour.
Who to Screen for Hepatitis B
The following groups should be tested for HBsAg, anti-HBs, and anti-HBc (the "HBV triple panel"):
| Risk Category | Details |
|---|---|
| Country of origin | All people born in HBV-endemic regions: East and Southeast Asia (China, Vietnam, Philippines, Cambodia, Korea), Pacific Islands (PNG, Fiji, Samoa, Tonga), sub-Saharan Africa, Central/South America, Middle East, Eastern Europe, Central Asia. HBV prevalence ≥2% in country of birth warrants testing. |
| Aboriginal and Torres Strait Islander peoples | Particularly those from remote and very remote communities in the NT, WA, and QLD where HBV prevalence is 3–6× the national average. Offer HBV serology as part of Adult Health Checks (MBS Item 715). |
| People who inject drugs (PWID) | Current or past injecting drug use — high prevalence of both HBV and HCV co-infection. Include those on opioid substitution therapy. |
| Men who have sex with men (MSM) | Higher rates of HBV acquisition through sexual transmission. |
| Household and sexual contacts of HBV carriers | Test for HBsAg, anti-HBs, anti-HBc; vaccinate if non-immune. |
| Pregnant women | HBsAg testing is recommended for all pregnancies (funded in most states/territories). Essential to identify candidates for neonatal immunoprophylaxis to prevent MTCT. |
| Haemodialysis patients | Screen at dialysis commencement and periodically (every 6–12 months). |
| Immunosuppression candidates | Prior to chemotherapy, biologics (anti-TNF, rituximab), or corticosteroid courses — risk of HBV reactivation. |
| HIV-positive individuals | Co-infection is common; test at HIV diagnosis and if unvaccinated. |
| Correctional facility inmates | High prevalence of HBV (and HCV); offer screening on reception. |
| Recipients of blood/tissue before 1990 | Prior to universal screening of blood products in Australia. |
Who to Screen for Hepatitis C
| Risk Category | Details |
|---|---|
| People who inject drugs (PWID) | Current or past injecting drug use — test at least annually; re-test every 6–12 months if ongoing risk. This is the single largest risk group in Australia. |
| Recipients of blood products before February 1990 | Before HCV screening of the Australian blood supply commenced. |
| Recipients of unscreened tissue/organs | Including those who received organs or tissues before HCV testing was routine. |
| Haemodialysis patients | Screen at commencement and every 6 months. |
| People living with HIV | Particularly MSM with HIV — rising incidence of sexually transmitted HCV in this population. |
| Children born to HCV-positive mothers | Maternal antibodies persist until 18 months; HCV PCR testing from 3 months of age, or anti-HCV after 18 months. |
| Inmates of correctional facilities | HCV prevalence 20–40% in Australian prisons. |
| Unexplained elevated ALT | Persistently elevated ALT after excluding alcohol, metabolic dysfunction-associated steatotic liver disease (MASLD), autoimmune, and drug causes. |
| Tattooing / body piercing in unregulated settings | Especially in correctional settings or overseas. |
Opt-out testing approach: For populations with high prevalence (e.g., PWID, correctional inmates, people from endemic countries), consider offering HBV/HCV testing as part of routine bloods without requiring explicit risk-factor disclosure. This reduces stigma and increases case detection.
MBS Item Numbers for Screening
- MBS Item 715 — Aboriginal and Torres Strait Islander Adult Health Check (includes viral hepatitis screening as a recommended component).
- MBS Item 69330 — Hepatitis B serology (HBsAg, anti-HBs, anti-HBc).
- MBS Item 69335 — Hepatitis C antibody.
- MBS Item 69345 — Hepatitis C RNA / PCR.
- MBS Item 721 / 723 — GP Management Plan / Team Care Arrangement — useful for chronic HBV patients requiring ongoing monitoring.
Initial Evaluation
Once a patient is identified as HBV or HCV seropositive, a structured initial evaluation is required to determine infection status, disease phase, degree of liver injury, and eligibility for antiviral therapy or specialist referral.
Hepatitis B — Serological Panel Interpretation
The initial HBV evaluation requires a "triple panel" plus supplementary tests:
| Test | MBS Item | Interpretation |
|---|---|---|
| HBsAg | 69330 | Positive = current infection (acute or chronic). Negative = no active infection. |
| Anti-HBs | 69330 | Positive (≥10 IU/L) = immune (vaccine-induced or natural). Negative = non-immune — consider vaccination. |
| Anti-HBc (total) | 69330 | Positive = past or current exposure. Negative = never infected. Isolated anti-HBc positivity may indicate resolved infection with waning anti-HBs, occult HBV, or false positive — check HBV DNA. |
| HBeAg | 69332 | Positive = active viral replication, high infectivity (immune-active or immune-tolerant phase). Negative = lower replication (may be immune-control or pre-core mutant). |
| Anti-HBe | 69332 | Positive = seroconversion (immune-control phase). Usually accompanies HBeAg loss. |
| HBV DNA (viral load) | 69342 | Quantitative PCR. Key for determining infection phase and treatment eligibility. >2,000 IU/mL generally indicates significant viral replication; >20,000 IU/mL typical of immune-active phase. |
| HBV genotype | 69342 | Useful for treatment planning (not always required). Genotype C predominant in Asian-born patients; genotype D in European/Middle Eastern; genotype A/C in ATSI communities. |
Interpreting the HBV Triple Panel — Common Patterns
| HBsAg | Anti-HBs | Anti-HBc | Interpretation |
|---|---|---|---|
| − | + | + | Past infection, immune. No further action unless immunosuppressed (check HBV DNA to exclude occult HBV). |
| − | + | − | Vaccine-induced immunity. Protected. |
| − | − | − | Non-immune, never infected. Vaccinate. |
| − | − | + | Isolated anti-HBc. Possible: resolved infection with waning anti-HBs, occult HBV, or false positive. Check HBV DNA; vaccinate if at ongoing risk. |
| + | − | + | Chronic HBV infection. Requires further evaluation (HBeAg, HBV DNA, LFTs, fibrosis assessment) and specialist referral. |
| + | − | − | Acute HBV (early). Rare in primary care — check IgM anti-HBc to distinguish from chronic. |
Hepatitis C — Antibody with Reflex PCR
HCV screening follows a two-step process:
1
HCV Antibody (anti-HCV)
Initial screening test (MBS 69335). A positive result indicates past or current exposure. It does not confirm active infection — up to 25% of infected individuals spontaneously clear the virus. Request reflex HCV PCR (RNA) at the time of ordering the antibody.
2
HCV RNA (PCR)
Confirmatory test for active infection (MBS 69345). Positive HCV RNA = active viraemia and treatment eligibility. Negative HCV RNA with positive antibody = past (resolved) infection — no treatment required, counsel re: meaning of "cleared". Undetectable RNA in a previously viraemic patient = sustained virological response (SVR = cure).
3
HCV Genotype
Determine genotype (1–6) to guide DAA regimen selection. Genotype 1 most common in Australia (~55%), followed by genotype 3 (~30%). Modern pangenotypic regimens (sofosbuvir/velpatasvir, glecaprevir/pibrentasvir) treat all genotypes, so genotyping is increasingly optional but still recommended.
Liver Function Tests (LFTs) & Baseline Bloods
For all patients with confirmed HBV or HCV infection, request:
- Liver function tests: ALT, AST, GGT, ALP, bilirubin, albumin — ALT is the most sensitive marker of hepatic inflammation in viral hepatitis.
- Full blood count (FBC): Low platelets may indicate advanced fibrosis/cirrhosis (portal hypertension).
- Coagulation studies: INR — elevated INR with low albumin suggests decompensated liver disease.
- Renal function (eGFR): Required before tenofovir (HBV) — nephrotoxic risk.
- HIV serology: All HBV/HCV-positive patients should be tested for HIV co-infection.
- Hepatitis A serology: Test for HAV IgG; vaccinate if non-immune (HAV superinfection in chronic liver disease carries high mortality).
- AFP: Baseline alpha-fetoprotein (useful for HCC surveillance but not diagnostic alone).
Fibrosis Assessment
Staging liver fibrosis is essential for prognosis and treatment decisions. Available tools in primary care:
GP Available
APRI Score (AST-to-Platelet Ratio Index)
Calculated from AST and platelet count. APRI <0.5 = low probability of significant fibrosis; APRI >1.5 = high probability of cirrhosis. Useful as a first-line screen in resource-limited settings. No cost (uses routine bloods).
GP Available
FIB-4 Index
Calculated from ALT, AST, platelet count, and age. FIB-4 <1.45 = low risk of advanced fibrosis; FIB-4 >3.25 = high risk. More accurate than APRI in patients >40 years. No cost.
Specialist / Referral
Transient Elastography (FibroScan®)
Non-invasive ultrasound-based measurement of liver stiffness. Gold standard non-invasive assessment. MBS Item 13035 (under hepatologist/gastroenterologist referral). KPa <7.0 = F0–F1 (mild); 7.0–9.5 = F2 (moderate); 9.5–12.5 = F3 (severe); >12.5 = F4 (cirrhosis). Thresholds vary by aetiology.
Specialist
Liver Biopsy
Gold standard for histological assessment but rarely required when non-invasive tests are concordant. Reserved for discordant non-invasive results, suspected dual pathology, or diagnostic uncertainty.
GP tip: Calculate APRI and FIB-4 using online calculators (e.g., hepfi.com or mdcalc.com) from routine pathology. If both scores suggest advanced fibrosis (F3–F4), prompt referral for FibroScan and specialist review is essential.
Pathophysiology
Hepatitis B
HBV is a partially double-stranded DNA virus (Hepadnaviridae family) that infects hepatocytes via the sodium taurocholate co-transporting polypeptide (NTCP) receptor. It replicates through an RNA intermediate (reverse transcriptase), resulting in the formation of covalently closed circular DNA (cccDNA) in the hepatocyte nucleus — a stable episomal reservoir that persists for the life of the cell and explains why HBV is rarely "cured" even after HBsAg loss.
Liver damage in HBV is predominantly immune-mediated — the virus itself is not directly cytopathic. Cytotoxic T lymphocyte (CTL) activity against infected hepatocytes drives hepatic inflammation and fibrosis. The balance between viral replication (immune-tolerant phase) and host immune clearance (immune-active phase) determines disease progression.
Natural History Phases of Chronic HBV
| Phase | HBeAg | HBV DNA | ALT | Liver Histology |
|---|---|---|---|---|
| Immune-tolerant | + | Very high (>10⁷ IU/mL) | Normal | Minimal inflammation/fibrosis |
| Immune-active (HBeAg+) | + | High (10⁴–10⁷ IU/mL) | Elevated (flares) | Moderate–severe inflammation, progressive fibrosis |
| Inactive carrier | − | Low (<2,000 IU/mL) | Normal | Variable — may have residual fibrosis |
| HBeAg-negative chronic hepatitis | − | Moderate–high (>2,000 IU/mL) | Elevated (fluctuating) | Active inflammation, progressive fibrosis — pre-core/basal core promoter mutants |
| HBsAg-negative (functional cure) | − | Undetectable (or very low cccDNA) | Normal | Resolved; may have residual fibrosis; HCC risk persists if cirrhosis was present |
Hepatitis C
HCV is a single-stranded RNA virus (Flaviviridae family) with 7 genotypes and >80 subtypes. It replicates in the cytoplasm of hepatocytes using the NS5B RNA-dependent RNA polymerase. Unlike HBV, HCV has no nuclear reservoir and no cccDNA equivalent — hence the possibility of complete virological cure (SVR).
HCV causes both direct cytopathic injury (via viral proteins and lipid metabolism disruption) and immune-mediated hepatocyte destruction. Chronic infection leads to progressive hepatic fibrosis over 20–30 years, with 10–20% of untreated patients developing cirrhosis. Established cirrhosis confers a 1–5% annual risk of HCC. Extrahepatic manifestations (mixed cryoglobulinaemia, membranoproliferative glomerulonephritis, porphyria cutanea tarda, non-Hodgkin lymphoma) are driven by chronic immune stimulation.
Clinical Presentation & Diagnostic Criteria
Acute Hepatitis B
- Incubation 45–160 days (mean 90 days).
- 70% of adults have subclinical or anicteric illness; 30% present with jaundice, malaise, nausea, RUQ pain, and hepatomegaly.
- Fulminant hepatic failure occurs in <1% — higher risk with HBV/HDV co-infection.
- Diagnosis: HBsAg+ and IgM anti-HBc+ (distinguishes acute from chronic flares).
- 95–99% of immunocompetent adults clear acute HBV spontaneously → HBsAg loss by 6 months.
Chronic Hepatitis B
- Most patients are asymptomatic for decades — detected only through screening.
- Non-specific symptoms when present: fatigue, RUQ discomfort, anorexia.
- Signs of advanced disease/cirrhosis: spider naevi, palmar erythema, jaundice, ascites, hepatosplenomegaly, gynaecomastia, caput medusae.
- Diagnosis: HBsAg positive for >6 months (or HBsAg+ on a single occasion with no clinical context suggesting acute infection, given most chronic carriers are asymptomatic).
Acute Hepatitis C
- Incubation 2–12 weeks (mean 6–7 weeks).
- 80% of cases are asymptomatic — rarely diagnosed in the acute phase.
- When symptomatic: mild fatigue, jaundice (uncommon), elevated ALT (often >10× ULN).
- Spontaneous clearance occurs in ~25% of acute infections (higher in females, IL28B CC genotype, symptomatic presentation).
Chronic Hepatitis C
- 75% of acute HCV infections become chronic.
- Most patients are asymptomatic for years to decades.
- Non-specific symptoms: fatigue, cognitive difficulties ("brain fog"), arthralgia, depression.
- Extrahepatic manifestations: mixed cryoglobulinaemia (vasculitis, purpura, arthralgia), membranoproliferative GN, porphyria cutanea tarda, type 2 diabetes (increased risk), B-cell non-Hodgkin lymphoma.
- Signs of cirrhosis as per HBV above.
- Diagnosis: anti-HCV positive + HCV RNA positive (PCR).
Do not use ALT to exclude chronic HBV or HCV. ALT may be persistently normal in 20–40% of patients with chronic hepatitis B or C, particularly in the inactive carrier phase (HBV) or indolent HCV. Normal ALT does not exclude significant fibrosis. Serological/virological testing is required for diagnosis.
Investigations
Summary of investigations for patients with confirmed HBV or HCV infection, including Australian availability and MBS funding:
Essential
HBsAg, anti-HBs, anti-HBc (triple panel)
MBS 69330. First-line serological assessment. Bulk-billed.
Essential
HBeAg / anti-HBe
MBS 69332. For HBsAg-positive patients — determines infection phase.
Essential
HBV DNA quantitative (viral load)
MBS 69342. Required for all HBsAg-positive patients to guide treatment decisions.
Essential
HCV antibody
MBS 69335. Request with reflex HCV RNA at time of ordering.
Essential
HCV RNA quantitative (PCR)
MBS 69345. Confirms active infection and measures viral load. Required for treatment eligibility.
Available
HCV genotype
MBS 69345. Guides DAA selection. Increasingly optional with pangenotypic regimens but still recommended.
Essential
LFTs (ALT, AST, GGT, ALP, bilirubin, albumin)
MBS 66500. Baseline and monitoring. ALT most sensitive for hepatic inflammation.
Essential
Full blood count (FBC)
MBS 66512. Thrombocytopenia suggests advanced fibrosis/portal hypertension.
Essential
INR / coagulation studies
MBS 66551. Baseline hepatic synthetic function.
Essential
eGFR / creatinine
Baseline renal function — particularly before tenofovir (HBV).
Available
APRI / FIB-4 (calculated)
Free — calculated from routine bloods. First-line non-invasive fibrosis screen.
Specialist
Transient elastography (FibroScan®)
MBS 13035 (specialist referral required). Non-invasive gold standard for fibrosis staging.
Available
HIV serology
MBS 69385. All HBV/HCV-positive patients. Essential before DAA initiation.
Available
HAV IgG
MBS 69360. Assess immunity; vaccinate if non-immune — critical before any liver disease.
Available
AFP + abdominal ultrasound
HCC surveillance for cirrhotic patients and HBV carriers ≥40 years (or with HCC family history). 6-monthly interval. US MBS 55106.
Risk Stratification & Severity Assessment
Hepatitis B Risk Stratification
The decision to treat chronic HBV is based on a combination of HBV DNA level, ALT, fibrosis stage, age, family history of HCC, and pregnancy status. Stratification guides urgency of specialist referral:
Low Priority
Inactive Carrier
HBeAg−, HBV DNA <2,000 IU/mL, persistently normal ALT, no/mild fibrosis (FIB-4 <1.45). Low short-term risk of progression.
Setting: GP surveillance — ALT + HBV DNA every 6–12 months; HCC screening 6-monthly US if ≥40 yrs or cirrhotic
Moderate Priority
Immune-Active / HBeAg-Negative Chronic Hepatitis
HBV DNA >2,000 IU/mL with elevated ALT (persistently >1× ULN) or moderate fibrosis (F2–F3). Significant risk of fibrosis progression.
Setting: Prompt specialist referral for antiviral eligibility assessment
High Priority
Compensated or Decompensated Cirrhosis / Immune-Active with High Viral Load
Any HBsAg+ patient with cirrhosis (F4), HBV DNA >20,000 IU/mL with elevated ALT, family history of HCC, or extrahepatic manifestations (polyarteritis nodosa, glomerulonephritis). Decompensation: ascites, variceal bleed, encephalopathy.
Setting: Urgent hepatology referral — treatment initiation even if ALT normal in cirrhotics
Treat all HBV patients with cirrhosis regardless of HBV DNA or ALT level. Any degree of cirrhosis is an indication for antiviral therapy. Refer urgently.
Hepatitis C — Treatment is Universal
Unlike HBV, all patients with detectable HCV RNA are eligible for DAA treatment — there are no ALT, fibrosis, or viral load thresholds required. The goal is universal treatment to achieve micro-elimmination. However, fibrosis staging remains important for:
- Determining treatment urgency (F3–F4 treated preferentially).
- Guiding DAA regimen duration (some regimens require 16 weeks for F4 or prior treatment failure).
- Post-SVR surveillance planning — patients with pre-treatment cirrhosis retain HCC risk and require lifelong 6-monthly surveillance.
| Fibrosis Stage | APRI | FIB-4 | FibroScan (KPa) | Treatment Urgency |
|---|---|---|---|---|
| F0–F1 (None–Mild) | <0.5 | <1.45 | <7.0 | Treat to prevent onward transmission and long-term complications |
| F2 (Moderate) | 0.5–1.5 | 1.45–3.25 | 7.0–9.5 | Treat promptly — fibrosis progressing |
| F3 (Severe) | >1.0 | >2.67 | 9.5–12.5 | Treat urgently — high risk of progression to cirrhosis |
| F4 (Cirrhosis) | >1.5 | >3.25 | >12.5 | Treat urgently — lifelong HCC surveillance required post-SVR |
Directed / Pathogen-Specific Therapy
Hepatitis C — Direct-Acting Antivirals (DAAs)
All Australians with chronic HCV (HCV RNA positive) are eligible for PBS-funded DAA treatment. Treatment is initiated by GPs (with s100 authority) or specialists. The choice of regimen depends on genotype, fibrosis stage, prior treatment history, and renal function.
Sofosbuvir / Velpatasvir (Epclusa®)
Gilead · Pangenotypic NS5B inhibitor + NS5A inhibitor
Adult dose
400/100 mg PO once daily for 12 weeks
Paediatric dose
≥6 years, ≥17 kg: weight-based dosing (sofosbuvir/velpatasvir granules or tablets)
Genotypes
All genotypes (1–6)
Renal adjustment
No dose adjustment. Can be used in eGFR <30 mL/min (unlike glecaprevir/pibrentasvir fixed-dose which contains tenofovir alafenamide — not recommended in eGFR <30 without close monitoring).
Hepatic adjustment
Contraindicated in decompensated cirrhosis (Child-Pugh B/C). Safe in compensated cirrhosis.
PBS status
✔ PBS Authority Required (s100)
Glecaprevir / Pibrentasvir (Mavyret®)
AbbVie · Pangenotypic NS3/4A protease inhibitor + NS5A inhibitor
Adult dose
300/120 mg (3 tablets) PO once daily with food for 8 weeks (treatment-naïve, non-cirrhotic); 12 weeks if compensated cirrhosis or prior treatment failure
Paediatric dose
≥12 years, ≥45 kg: adult dosing; granules available for younger children
Genotypes
All genotypes (1–6)
Renal adjustment
No adjustment required including eGFR <30 mL/min and dialysis patients.
Hepatic adjustment
Contraindicated in decompensated cirrhosis (Child-Pugh B/C).
PBS status
✔ PBS Authority Required (s100)
Cure rates >95%. Both pangenotypic regimens achieve SVR (sustained virological response = cure) in >95% of patients, including those with compensated cirrhosis, HIV co-infection, and prior treatment failure. SVR12 (HCV RNA undetectable 12 weeks post-treatment) confirms cure.
Hepatitis B — Nucleos(t)ide Analogues
Treatment of chronic HBV is initiated by or in consultation with a hepatologist, gastroenterologist, or infectious disease specialist. The goal is viral suppression (HBV DNA undetectable), not cure — long-term (often indefinite) therapy is required. First-line agents are:
Tenofovir disoproxil (Viread®)
Gilead · Nucleotide analogue — HBV DNA polymerase inhibitor
Adult dose
245 mg PO once daily (with or without food)
Key notes
First-line agent (equally efficacious as entecavir). Monitor renal function (eGFR) and phosphate at baseline, 3-monthly for first year, then annually. Risk of Fanconi syndrome and reduced bone mineral density with long-term use.
Renal adjustment
eGFR 30–49: 245 mg every 48 hours. eGFR 10–29: 245 mg every 72–96 hours. HD: 245 mg after each session. Consider tenofovir alafenamide (TAF) for renal protection.
PBS status
✔ PBS Authority Required (s100)
Entecavir (Baraclude®)
BMS · Nucleoside analogue — HBV DNA polymerase inhibitor
Adult dose
0.5 mg PO once daily on empty stomach (at least 2 hours from food)
Key notes
First-line agent with high barrier to resistance. Preferred in patients with renal concerns (less nephrotoxic than tenofovir disoproxil). Avoid in lamivudine-experienced patients (higher resistance rate; use 1 mg dose).
Renal adjustment
eGFR 30–49: 0.5 mg every 48 hours. eGFR 10–29: 0.5 mg every 72 hours. HD/CAPD: 0.5 mg weekly.
PBS status
✔ PBS Authority Required (s100)
Never stop HBV antivirals abruptly without specialist input. Sudden withdrawal of nucleos(t)ide analogues can precipitate a severe hepatitis flare (immune reconstitution) leading to hepatic decompensation and death. Lifelong therapy is often required — if cessation is considered, it must be under hepatology supervision with close post-cessation monitoring.
HBV Treatment Indications (Summary for Referral)
| Indication for Treatment | Criteria |
|---|---|
| Cirrhosis | Any HBsAg+ patient with cirrhosis, regardless of HBV DNA or ALT — treat immediately |
| Immune-active HBeAg+ chronic hepatitis | HBV DNA >20,000 IU/mL AND ALT >2× ULN persisting >3–6 months |
| HBeAg-negative chronic hepatitis | HBV DNA >2,000 IU/mL AND ALT >1× ULN persisting >3–6 months |
| Family history of HCC | Lower thresholds for treatment — discuss with specialist even with normal ALT |
| Extrahepatic manifestations | Polyarteritis nodosa, HBV-associated GN |
| Immunosuppression planned | Prophylactic antiviral before and during immunosuppressive therapy (chemotherapy, biologics, high-dose corticosteroids) to prevent reactivation |
| Pregnancy — high viral load | HBV DNA >200,000 IU/mL in 3rd trimester — tenofovir from 28–32 weeks gestation to prevent MTCT |
HBV Vaccination for Non-Immune Contacts
All susceptible (anti-HBs <10 IU/L) household and sexual contacts of HBV carriers should receive hepatitis B vaccination:
Hepatitis B Vaccine (Engerix-B®, H-B-Vax II®)
GSK / CSL Seqirus · Recombinant HBsAg vaccine
Adult dose
20 µg IM deltoid — 3-dose schedule at 0, 1, and 6 months (accelerated 0, 1, 2 months + booster at 12 months available for travellers/urgent situations)
Paediatric dose
10 µg IM (paediatric formulation) — NIP schedule: birth dose + 2, 4, 6 months
Post-vaccination serology
Check anti-HBs 4–8 weeks after completing course. Target ≥10 IU/L. Non-responders: repeat full course or give double dose (40 µg). Booster doses generally not required in immunocompetent individuals who achieved seroconversion.
PBS status
✔ NIP (funded for infants, adolescents, ATSI adults, high-risk groups)
If a non-immune sexual contact of an HBV carrier presents within 72 hours of a high-risk exposure, consider hepatitis B immunoglobulin (HBIG) in addition to commencing vaccination.
Monitoring
Chronic Hepatitis B — Long-Term Monitoring
Every 6–12 months
Inactive carriers (HBeAg−, HBV DNA <2,000 IU/mL, normal ALT): ALT every 6 months for first year then every 6–12 months; HBV DNA annually. Any ALT elevation warrants repeat HBV DNA — phase reactivation occurs in 20–30% of carriers.
Every 3–6 months
On antiviral therapy: HBV DNA, ALT, HBeAg/anti-HBe at 3-monthly intervals until undetectable HBV DNA achieved, then every 6 months. Renal function (eGFR) and serum phosphate at baseline, 3-monthly for first year (tenofovir), then annually.
Every 6 months (lifelong)
HCC surveillance: Abdominal ultrasound ± AFP every 6 months for all patients with cirrhosis, and for non-cirrhotic HBV carriers aged ≥40 years, or any age with family history of HCC, or high HBV DNA (>2,000 IU/mL) with ongoing inflammation.
Annually
Fibrosis reassessment: APRI/FIB-4 annually; FibroScan every 2–3 years or if clinical concern.
Hepatitis C — Post-Treatment Monitoring
Week 12 post-treatment
SVR12 confirmatory HCV RNA: Undetectable = sustained virological response (cure). This is the primary endpoint of DAA therapy.
Post-SVR — no cirrhosis
Annual LFTs for 2 years then per GP discretion. If ongoing risk factors (PWID), re-test HCV RNA annually for reinfection. No further HCC surveillance required.
Post-SVR — with cirrhosis (F4)
Lifelong 6-monthly HCC surveillance with abdominal ultrasound ± AFP. HCC risk persists post-cure in cirrhotics. Also ensure gastroscopy screening for varices if not already performed. LFTs every 6 months.
Post-SVR — PWID
Annual HCV RNA to detect reinfection (2–8% per year risk). Reinfection does not mean treatment failure — retreat with same DAA regimen is effective.
GP follow-up is appropriate post-cure for patients without cirrhosis. Patients with cirrhosis (pre-treatment F4) require ongoing specialist HCC surveillance regardless of SVR status.
Special Populations
Pregnancy
HBV — prevention of MTCT:
All pregnant women should be screened for HBsAg. If HBV DNA >200,000 IU/mL, commence tenofovir disoproxil 245 mg PO daily from 28–32 weeks gestation, continuing until 4 weeks postpartum (or ongoing if treatment-indicated). Neonatal immunoprophylaxis (HBIG + HBV vaccine within 12 hours of birth) is essential regardless of maternal viral load.
HCV — treatment deferral:
DAAs are not currently approved in pregnancy. Defer DAA treatment until postpartum. HCV does not affect pregnancy management significantly but increases risk of cholestasis. Breastfeeding is safe unless nipples are cracked/bleeding.
Tenofovir in pregnancy:
Tenofovir disoproxil is Category B3 in pregnancy. Extensive safety data from HIV use. Benefits of preventing MTCT outweigh risks.
Paediatrics
HBV in children:
Children infected perinatally are typically in the immune-tolerant phase (high HBV DNA, normal ALT, minimal fibrosis). Treatment is generally deferred unless there is evidence of significant hepatitis or fibrosis. Referral to paediatric hepatology is essential. HBV vaccination on the NIP schedule (birth, 2, 4, 6 months) with post-vaccination serology at 12 months for babies born to HBV-positive mothers.
HCV in children:
Born to HCV-positive mothers: test HCV RNA at 3 months of age (anti-HCV maternal antibodies persist until 18 months). Spontaneous clearance occurs in ~25–40% by age 3. If HCV RNA persists >3 years, consider DAA treatment. Glecaprevir/pibrentasvir approved ≥3 years; sofosbuvir/velpatasvir ≥6 years. Refer to paediatric hepatology.
Elderly
HBV:
Higher prevalence of HBeAg-negative chronic hepatitis (pre-core mutants) in older patients — may present with fluctuating ALT and moderate HBV DNA. Increased HCC risk with age and duration of infection — ensure 6-monthly ultrasound surveillance. Monitor renal function closely on tenofovir — consider entecavir or tenofovir alafenamide if renal concerns.
HCV:
DAAs are equally effective in older adults. Drug interactions more common — review concomitant medications (statins, anticoagulants, PPIs). Older patients with advanced fibrosis should be treated urgently as progression accelerates with age.
Renal Impairment
HBV:
Tenofovir disoproxil is nephrotoxic — requires dose adjustment and close monitoring (eGFR, phosphate, bicarbonate) in CKD. If eGFR <30 mL/min, consider entecavir (preferred) or tenofovir alafenamide (TAF) — less renal toxicity. Haemodialysis patients: entecavir dosed post-dialysis.
HCV:
Glecaprevir/pibrentasvir is preferred in eGFR <30 mL/min (no renal dose adjustment). Sofosbuvir/velpatasvir can also be used. Avoid sofosbuvir-based regimens in dialysis patients unless no alternative (limited data for eGFR <15 mL/min with sofosbuvir). Treatment of HCV in CKD may improve renal function.
Hepatic Impairment
HBV — decompensated cirrhosis:
Entecavir or tenofovir can be used in decompensated cirrhosis under specialist supervision. Monitor for lactic acidosis. Refer for transplant assessment if Child-Pugh ≥C or MELD ≥15.
HCV — decompensated cirrhosis:
DAAs containing NS3/4A protease inhibitors (glecaprevir, voxilaprevir, paritaprevir) are contraindicated in Child-Pugh B/C. Use sofosbuvir/velpatasvir + ribavirin under specialist guidance for 12 weeks. Sofosbuvir/daclatasvir is an alternative.
Immunocompromised
HBV reactivation risk:
Screen ALL patients before starting immunosuppressive therapy (anti-TNF, rituximab, chemotherapy, high-dose corticosteroids >4 weeks). If HBsAg+ or isolated anti-HBc+ with high-risk immunosuppression (rituximab, stem cell transplant), commence prophylactic antiviral (entecavir or tenofovir) before treatment, continuing for ≥12 months after cessation (≥18 months for rituximab). Monitor HBV DNA during therapy.
HCV + HIV co-infection:
DAAs are equally effective in HIV co-infection. Check for drug–drug interactions with antiretrovirals (particularly with glecaprevir/pibrentasvir and certain HIV protease inhibitors). DAA treatment should not be delayed — treat HCV regardless of CD4 count.
Post-transplant:
HBV/HCV treatment in transplant recipients requires specialist management. Sofosbuvir/velpatasvir or glecaprevir/pibrentasvir are preferred post-liver transplant for HCV recurrence.
Aboriginal and Torres Strait Islander Health
Aboriginal and Torres Strait Islander Health Considerations
Action for GPs: If you have Aboriginal and Torres Strait Islander patients with chronic HBV who are not receiving 6-monthly HCC surveillance or who have not been linked to a liver specialist, make this a priority. HCC is preventable with timely surveillance and treatment — and the burden falls disproportionately on Indigenous Australians.
📚 References
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