Hepatitis D, E & G

📋 Key Information Summary

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Hepatitis D (HDV) is an incomplete RNA virus that requires hepatitis B virus (HBV) co-infection to replicate — test all HBsAg-positive patients for anti-HDV at least once during their clinical course.
Two patterns: co-infection (simultaneous acute HBV + HDV — usually self-limiting) vs superinfection (pre-existing chronic HBV acquiring HDV — high chronicity rate >80%, accelerated fibrosis, rapid cirrhosis).
HDV accelerates liver disease progression 3–5-fold compared with HBV alone; it is the most severe form of chronic viral hepatitis.
Treatment options for HDV: bulevirtide (entry inhibitor, PBS Authority Required), pegylated interferon alfa-2a (48-week course), plus ongoing HBV nucleos(t)ide antiviral (entecavir or tenofovir) — all regimens require specialist management.
Hepatitis E (HEV) genotypes 1 and 2 are water-borne, endemic in South Asia and sub-Saharan Africa; genotype 1 causes severe disease in pregnancy with mortality up to 25 % (fulminant hepatic failure).
HEV genotypes 3 and 4 are zoonotic (undercooked pork, game meat), the dominant genotypes in Australia; genotype 3 can cause chronic infection in immunocompromised hosts (solid-organ transplant, haematopoietic stem-cell transplant, advanced HIV).
Diagnose HEV with IgM anti-HEV (acute) and HEV RNA PCR (chronic or immunocompromised); genotype 3 chronic HEV is treated with ribavirin (600 mg PO daily × 12 weeks; PBS Authority Required).
For immunocompromised patients with chronic HEV, first reduce immunosuppression before starting ribavirin.
Hepatitis G virus (GBV-C) is a pegivirus — a common bloodborne virus with no proven causal link to clinical hepatitis; routine testing is not recommended.
GBV-C co-infection in HIV-positive individuals is associated with slower disease progression and reduced mortality — an immunomodulatory effect, not a therapeutic indication.
Aboriginal and Torres Strait Islander peoples have higher HBV prevalence (and therefore higher HDV risk); ensure culturally safe testing, notification to jurisdictional health departments, and engagement with local Aboriginal Community Controlled Health Organisations (ACCHOs).
All three hepatitis viruses require mandatory notification to state/territory health departments under Australian public-health legislation.
Travellers to endemic regions should be counselled on safe water and food hygiene (HEV D/E prevention); HBV vaccination remains the cornerstone of HDV prevention.

Introduction & Australian Epidemiology

Beyond hepatitis A, B, and C, three additional hepatitis viruses — D, E, and G — contribute to liver disease in Australia, though each has a distinct epidemiology, clinical significance, and management paradigm. Understanding these agents is essential for comprehensive viral-hepatitis care in primary and specialist settings.

Hepatitis D (HDV)

HDV is a small, defective RNA virus (genus Deltavirus) that requires the HBV surface antigen (HBsAg) for assembly and transmission. Australia has a low but non-trivial prevalence of HDV, estimated at 1–5 % of HBsAg carriers. Risk groups include people who inject drugs (PWID), migrants from HDV-endemic regions (Mongolia, Central Africa, Eastern Mediterranean, Amazon basin), and men who have sex with men (MSM). In 2022–23, Australian sentinel surveillance identified increasing HDV awareness but persistent under-testing.

Hepatitis E (HEV)

HEV is the most common cause of acute viral hepatitis worldwide. In Australia, autochthonous genotype 3 infections from undercooked pork products (including pork liver pâté, salami, and wild boar) are increasingly recognised. Imported genotype 1/2 infections occur in returned travellers from South and South-East Asia. HEV notification rates have risen from <20 per year (pre-2010) to >100 per year nationally, reflecting improved diagnostics.

Hepatitis G (GBV-C)

GBV-C is a flavivirus-related pegivirus found in 1–4 % of Australian blood donors. It is parenterally transmitted and shares risk factors with HIV and hepatitis C virus (HCV). Despite its name, GBV-C has never been convincingly shown to cause hepatitis in humans. It is primarily of academic interest, though its interaction with HIV has generated significant research attention.

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Mandatory notification: In all Australian states and territories, hepatitis D, E, and G (where identified) are notifiable conditions. Positive results must be reported to the relevant communicable-disease branch.

Hepatitis D

Virology & Requirement for HBV Co-infection

HDV is a 36 nm, single-stranded, circular RNA virus with an envelope derived from HBV surface antigens. It cannot replicate independently — it hijacks HBsAg production for virion assembly. Consequently, HDV infection only occurs in individuals who are HBsAg-positive, either as a simultaneous co-infection or as a superinfection of pre-existing chronic HBV.

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Screening recommendation: Test all HBsAg-positive patients for anti-HDV antibody (IgG/IgM) at least once during their clinical course. If anti-HDV positive, proceed to HDV RNA PCR to confirm active replication. Repeat testing may be warranted in high-risk groups (PWID, migrants from endemic regions, MSM).

Co-infection vs Superinfection

Feature	Co-infection (acute HBV + HDV)	Superinfection (chronic HBV + new HDV)
Setting	Simultaneous acute infection with both viruses in a previously HBV-naïve patient	Pre-existing chronic HBV acquires HDV
Clinical course	Usually biphasic hepatitis; majority (>90 %) resolve both HBV and HDV spontaneously	Acute hepatitis flare; chronicity develops in >80 % of cases
Fulminant risk	1–3 % (higher than HBV alone)	5–10 % during acute flare
Chronicity	<5 %	>80 %
Fibrosis progression	If chronic: accelerated (3–5 × HBV alone)	Rapid — cirrhosis within 5–10 years in 70–80 % if untreated
HCC risk	Increased if chronic	Significantly elevated; surveillance every 6 months with AFP + ultrasound

Diagnostic Pathway

1

HBsAg confirmed positive

All HBsAg-positive patients should be tested for anti-HDV total antibody (IgG ± IgM).

2

Anti-HDV positive

Proceed to HDV RNA qualitative PCR (available through reference laboratories — VIDRL Melbourne, Westmead ICPMR). Quantitative HDV RNA may be used for treatment monitoring.

3

HDV RNA positive

Active HDV replication confirmed. Assess liver fibrosis (FibroScan®, enhanced liver fibrosis [ELF] test, or liver biopsy). Refer to hepatologist/gastroenterologist.

4

Treatment decision

Specialist-directed: bulevirtide, pegylated interferon, or combination. Continue HBV nucleos(t)ide analogue throughout.

Treatment of Hepatitis D

Treatment of HDV is complex and should be managed by a hepatologist or infectious-disease specialist experienced in viral hepatitis. Three therapeutic strategies are available in Australia:

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Bulevirtide (Hepcludex®)

Entry inhibitor · Anti-NTCP (sodium-taurocholate co-transporting polypeptide)

Mechanism Blocks HBV/HDV entry into hepatocytes by binding NTCP receptor

Adult dose 2 mg SC daily (self-administered); minimum 48 weeks, often ≥96 weeks

Paediatric dose Not established — specialist use only in adolescents ≥12 years on a case-by-case basis

Renal adjustment Not required (no significant renal excretion)

Hepatic adjustment Use with caution in decompensated cirrhosis (Child-Pugh B/C) — limited data

Key adverse effects Injection-site reactions, pruritus, transient ALT elevations

PBS status ⛔ Authority Required — Specialist (TGA registered, PBS listing pending/compassionate use)

Note TGA-registered since 2023. Obtain through Special Access Scheme (SAS Category B) or compassionate-use programme if PBS listing unavailable. Always combine with HBV nucleos(t)ide analogue (entecavir or tenofovir) to suppress HBV.

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Pegylated interferon alfa-2a (Pegasys®)

Immunomodulator · Antiviral

Adult dose 180 µg SC once weekly × 48 weeks

Efficacy HDV RNA suppression in ~25–30 %; durability of response variable (relapse in 40–50 %)

Key adverse effects Flu-like symptoms, cytopenias, depression, thyroid dysfunction, autoimmune phenomena

Contraindications Decompensated cirrhosis, severe psychiatric illness, autoimmune hepatitis, pregnancy

Renal adjustment Reduce dose to 135 µg/week if eGFR <30 mL/min/1.73 m²

PBS status ⚠ PBS Restricted Benefit — chronic hepatitis D (specialist authority)

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Entecavir (Baraclude®)

Nucleoside analogue · HBV suppression backbone

Adult dose 0.5 mg PO daily (treatment-naïve) or 1 mg PO daily (lamivudine-resistant)

Role in HDV Continued alongside bulevirtide or peg-IFN to suppress HBV replication — does NOT treat HDV directly

Renal adjustment Yes — reduce dose for CrCl <50 mL/min (consult product information)

PBS status ✔ PBS General Benefit

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Tenofovir disoproxil fumarate (Viread®) / Tenofovir alafenamide (Vemlidy®)

Nucleotide analogue · HBV suppression backbone

Adult dose TDF 300 mg PO daily; TAF 25 mg PO daily

Role in HDV Alternative HBV backbone; preferred in patients with renal impairment or osteoporosis (TAF)

Renal adjustment TDF: contraindicated if CrCl <15 mL/min; TAF: no adjustment required (preferred in CKD)

PBS status ✔ PBS General Benefit

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Critical: Never stop HBV nucleos(t)ide analogue therapy when treating HDV with bulevirtide or peg-IFN. Ceasing the HBV backbone risks HBV reactivation, which may precipitate hepatic decompensation — sometimes fatal.

Monitoring During HDV Treatment

ALT and quantitative HDV RNA at weeks 12, 24, 48, and then every 24 weeks.
HBV DNA every 12–24 weeks (ensure continued HBV suppression).
FBC, thyroid function, and psychiatric screening (monthly for first 3 months) if on peg-IFN.
Liver elastography (FibroScan®) annually to monitor fibrosis regression.
HCC surveillance (AFP + liver ultrasound every 6 months) in all patients with established cirrhosis.

Prevention of Hepatitis D

HBV vaccination is the most effective prevention — HDV cannot establish infection without HBV.
Ensure all HBsAg-negative contacts of HDV patients are vaccinated against HBV.
Harm-reduction counselling for PWID: needle-syringe programmes, safe injecting education.
Screen blood and organ donations for HBsAg (already standard in Australian Blood Service).

Hepatitis E

Virology & Genotypes

HEV is a single-stranded, positive-sense RNA virus (family Hepeviridae). Four genotypes of clinical significance are recognised:

Genotype	Transmission	Endemic regions	Key clinical features
1	Faecal–oral (contaminated water)	South Asia, North/West Africa	Large outbreaks; severe in pregnancy (mortality up to 25 %); self-limiting in immunocompetent
2	Faecal–oral (contaminated water)	Central America, West Africa	Similar to genotype 1; outbreaks in displaced populations
3	Zoonotic (pork, game meat)	Europe, Australia, Japan, USA	Predominant genotype in Australia; usually self-limiting; chronic in immunocompromised
4	Zoonotic (pork)	East/South-East Asia	Less common in Australia; sporadic; older-age predominance; chronic infection rare

Clinical Presentation

In immunocompetent adults, HEV genotype 3 typically causes a self-limiting acute hepatitis with jaundice, malaise, nausea, and right-upper-quadrant discomfort. The incubation period is 2–8 weeks. Most patients recover fully within 4–6 weeks without antiviral therapy.

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Pregnancy warning: HEV genotype 1 infection in the second or third trimester carries a case-fatality rate of up to 25 %, predominantly from fulminant hepatic failure and haemorrhagic complications. Pregnant travellers returning from endemic areas with acute hepatitis should be urgently tested for HEV.

Chronic HEV in Immunocompromised Patients

Chronic HEV (HEV RNA positivity >3 months) is recognised almost exclusively with genotype 3 and occurs in:

Solid-organ transplant recipients on calcineurin inhibitors (tacrolimus, ciclosporin) — prevalence 0.5–2 % in European/Australian cohorts.
Haematopoietic stem-cell transplant recipients.
Patients with advanced HIV (CD4 <200 cells/µL).
Patients on rituximab or other anti-CD20 therapies.

Chronic HEV can lead to progressive hepatic fibrosis and cirrhosis within 2–3 years if untreated. Extrahepatic manifestations include neurological disease (neuralgic amyotrophy, Guillain-Barré syndrome, encephalitis), membranous nephropathy, and haematological cytopenias.

Diagnosis

Available IgM anti-HEV (acute serology) Sensitivity 90–95 % in immunocompetent; may be falsely negative in immunocompromised. Available through major pathology labs (Sullivan Nicolaides, Douglass Hanly Moir, SA Pathology).

Available IgG anti-HEV (past exposure) Sero-epidemiological marker; does not distinguish acute from past infection. Useful in returned-traveller assessment.

Reference lab HEV RNA (qualitative/quantitative PCR) Gold standard for active infection. Essential in immunocompromised patients (serology unreliable). Available through VIDRL (Melbourne), Westmead ICPMR, QML reference. MBS item: referral-level testing.

Available Liver function tests (ALT, bilirubin, INR) Acute hepatitis: ALT typically 500–3000 IU/L. Monitor INR for fulminant-course prediction.

Treatment

Mild–Moderate

Acute HEV (immunocompetent)

Self-limiting in >95 % of cases. Supportive care: hydration, anti-emetics, avoid hepatotoxins (alcohol, paracetamol excess). Monitor LFTs weekly until resolution.

Setting: GP / outpatient

Moderate

Chronic HEV (immunocompromised) — initial

Step 1: Reduce immunosuppression (especially tacrolimus, mycophenolate). Reassess HEV RNA at 3 months. Many patients (>30 %) clear virus with immunosuppression reduction alone.

Setting: Transplant ID / hepatologist

Severe

Chronic HEV refractory / acute severe / pregnancy

Ribavirin 600 mg PO daily × 12 weeks (extend to 24 weeks if partial response). Monitor HEV RNA at weeks 4, 8, 12. If ribavirin fails: pegylated interferon alfa (specialist only).

Setting: Specialist hepatology unit / transplant centre

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Ribavirin (Copegus® / Virazole®)

Nucleoside analogue · Antiviral

Adult dose — chronic HEV 600 mg PO daily (fixed dose) OR weight-based: <75 kg → 400 mg AM + 200 mg PM; ≥75 kg → 400 mg BD. Duration: 12 weeks minimum, extend to 24 weeks if HEV RNA declining but not cleared.

Adult dose — acute severe HEV 600 mg PO daily × 12 weeks (limited evidence; specialist decision)

Paediatric dose Not established for HEV. Limited case reports in adolescents at 15 mg/kg/day divided BD — specialist use only.

Renal adjustment CrCl 30–50 mL/min: 200 mg BID; CrCl <30 mL/min: 200 mg daily; haemodialysis: 200 mg after dialysis. Use with extreme caution.

Key adverse effects Haemolytic anaemia (monitor Hb fortnightly), teratogenicity (Category X — effective contraception required in both sexes during and 7 months after treatment), fatigue, cough

PBS status ⛔ Authority Required — specialist (chronic HEV in immunocompromised patients)

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Teratogenicity: Ribavirin is Category X — absolutely contraindicated in pregnancy. Ensure pregnancy testing before initiation and enforce reliable contraception in female patients of childbearing potential and in male partners (drug present in seminal fluid) during treatment and for 7 months post-cessation.

Prevention of Hepatitis E

Food safety: cook pork and game meat thoroughly (core temperature ≥70 °C); avoid raw/undercooked pork liver, salami, and wild boar.
Water safety: drink treated/boiled water when travelling to endemic regions (South Asia, Africa).
No licensed HEV vaccine is available in Australia (HEV 239 vaccine licensed in China only).
Screen donated blood and organs — Australian Red Cross Lifeblood introduced HEV screening (minipool NAT) in 2023.
Counsel immunocompromised patients (especially transplant recipients) to avoid raw/undercooked pork products.

Hepatitis G (GBV-C / HGV)

Virology

Hepatitis G virus — also known as GB virus C (GBV-C) — is a single-stranded RNA virus of the genus Pegivirus within the family Flaviviridae. Despite its historical name, GBV-C is not a hepatotropic virus and has never been convincingly demonstrated to cause hepatitis or any other liver disease in humans.

Epidemiology

GBV-C is a common bloodborne virus; seroprevalence is 1–4 % in Australian blood donors and up to 15–20 % in high-risk populations (PWID, haemodialysis patients, recipients of multiple transfusions).
Transmission routes: parenteral (blood products, injecting drug use), sexual, and vertical (mother-to-child).
Co-infection with HCV is common (20–30 % of HCV-positive individuals) and with HIV (15–40 %).
Persistent viraemia occurs in ~25 % of infected individuals; the remainder clear the virus spontaneously.

Clinical Significance

❌ Not clinically significant for hepatitis

No association with acute or chronic hepatitis
No association with hepatocellular carcinoma
No association with cirrhosis or liver fibrosis
Does not alter the course of HBV or HCV co-infection in a clinically meaningful way

🔬 Research interest: HIV interaction

GBV-C co-infection in HIV-positive individuals is associated with slower CD4 decline, reduced HIV viral load, and lower mortality — a paradoxical protective effect
Proposed mechanisms: down-regulation of HIV co-receptors (CCR5, CXCR4), modulation of cytokine milieu, T-cell homeostasis
Clinical application: none at present — GBV-C is not recommended as a therapeutic agent for HIV
GBV-C clearance (spontaneous or treatment-induced) in HIV co-infected patients may paradoxically worsen HIV outcomes — a research observation, not a clinical recommendation

Testing Recommendations

ℹ️

Routine GBV-C testing is NOT recommended in any clinical scenario. GBV-C RNA and anti-E2 antibody testing are available only through specialised research/reference laboratories and should be reserved for epidemiological studies or specific research protocols. There is no MBS item for routine GBV-C testing. The presence of GBV-C should not alter management of HBV, HCV, HIV, or any liver disease.

Management

No treatment is indicated for GBV-C infection. No antiviral therapy has demonstrated efficacy against GBV-C, and none is recommended. Patients found to have incidental GBV-C viraemia should be reassured that it is a benign finding and does not require follow-up, treatment, or referral.

✅

Reassurance for patients: If GBV-C is incidentally detected (e.g., through blood-donation screening or research testing), explain that it is a harmless virus — likened to having a common commensal organism. No lifestyle modification, treatment, or specialist referral is required.

Special Populations

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Pregnancy

HDV

Pegylated interferon is contraindicated in pregnancy. Bulevirtide: no human pregnancy data — avoid unless life-threatening HDV. Continue HBV nucleos(t)ide analogue (tenofovir preferred) to prevent HBV perinatal transmission. Caesarean section not indicated solely for HDV.

HEV Genotype 1

Highest priority: Mortality up to 25 % in 2nd/3rd trimester. Urgent hepatology referral. Supportive care; ribavirin absolutely contraindicated (Category X). Monitor closely for fulminant hepatic failure — early transfer to liver-transplant centre if INR rising or encephalopathy develops.

HEV Genotype 3

Usually self-limiting. Supportive care. Ribavirin contraindicated.

GBV-C

No clinical significance. No action required.

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Paediatrics

HDV

Rare in children. Superinfection may occur in HBV-infected children (especially endemic-migrant families). Bulevirtide: not established in children <12 years. Peg-IFN: limited data; specialist management only. HBV vaccination of all children remains the primary prevention strategy (NIP schedule).

HEV

Genotype 3 usually causes anicteric or mild hepatitis in children. Chronic HEV exceptionally rare in immunocompetent paediatric patients. Ribavirin: no established paediatric dose for HEV; specialist consultation required.

GBV-C

May be vertically transmitted. No clinical significance.

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Elderly

HDV / HEV / GBV-C

Ageing liver has reduced regenerative capacity; accelerated fibrosis from HDV superinfection is particularly dangerous. Ribavirin-associated haemolytic anaemia is more likely in elderly patients — monitor FBC closely. Peg-IFN side-effect profile (depression, cytopenias) is less well tolerated — consider bulevirtide as first-line in eligible patients.

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Renal Impairment

Ribavirin (HEV)

Significant dose reduction required (see drug card above). Accumulates and worsens anaemia in CKD. Haemodialysis patients: give 200 mg after dialysis session. Avoid if possible in CKD stage 5.

Entecavir (HDV backbone)

Dose adjustment required for CrCl <50 mL/min. Tenofovir alafenamide (TAF) preferred over tenofovir disoproxil (TDF) in CKD.

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Hepatic Impairment

Bulevirtide

Limited data in decompensated cirrhosis (Child-Pugh B/C). Use with extreme caution; monitor for worsening hepatic function. Peg-IFN contraindicated in decompensated disease.

Ribavirin

No specific hepatic adjustment; however, synthetic dysfunction (low albumin, elevated INR) increases risk of ribavirin toxicity. Specialist hepatology involvement essential.

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Immunocompromised

HDV

HDV disease course generally similar to immunocompetent; treatment response to peg-IFN may be impaired. Bulevirtide mechanism (entry blockade) is not immunosuppression-dependent — preferred agent in this group.

HEV

Key population: Transplant recipients at risk of chronic HEV genotype 3. Stepwise approach: (1) reduce immunosuppression, (2) ribavirin if persistent viraemia at 3 months, (3) peg-IFN as last resort. Avoid HEV testing with serology alone — always use HEV RNA PCR (serology unreliable with impaired humoral immunity).

GBV-C

No clinical significance, even in immunocompromised hosts.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

HBV prevalence

Aboriginal and Torres Strait Islander peoples have a chronic HBV prevalence of 3–6 % — approximately 3–5 times higher than the non-Indigenous Australian population. Given that HDV requires HBV, the pool at risk of HDV superinfection is proportionally larger.

HDV screening gaps

HDV testing rates among Indigenous HBsAg-positive patients are suboptimal. Ensure anti-HDV testing is performed at least once for every Indigenous HBsAg-positive individual. Integrate HDV screening into existing chronic-disease management programmes and Aboriginal Community Controlled Health Organisation (ACCHO) hepatitis-care pathways.

HEV risk — remote and very remote communities

Hunting and consumption of feral pig (wild boar) meat is common in some remote NT, QLD, and WA communities. Feral pigs are a known reservoir for HEV genotype 3. Provide culturally appropriate education on safe meat handling and thorough cooking of game meat.

HBV vaccination — NIP coverage

HBV vaccination (NIP-funded at birth, 2 months, 6 months) remains the most effective HDV prevention strategy. In some remote communities, vaccination timeliness may lag. Outreach immunisation programmes through ACCHOs should prioritise HBV catch-up vaccination, particularly for adolescents and young adults.

Specialist access

Hepatology and infectious-disease specialist services for HDV/HEV treatment are concentrated in metropolitan centres. Telehealth (MBS items 91822, 91823) and visiting-specialist programmes are essential. The RHDAustralia guidelines and state/territory hepatitis programmes provide care models for remote viral-hepatitis management.

Cultural safety

Discuss hepatitis testing within a culturally safe framework — use Aboriginal Health Workers/Practitioners as intermediaries. Acknowledge the social and historical determinants of health that contribute to higher hepatitis prevalence. Respect kinship structures and gender-appropriate care preferences. Follow the National Safety and Quality Health Service (NSQHS) Standards for culturally safe care.

Stigma & disclosure

Hepatitis diagnoses carry significant stigma in small, close-knit communities. Ensure confidentiality; discuss with patients who should be informed. Use non-judgemental, strengths-based language. Link with local ACCHO-based hepatitis-support workers.

Data & surveillance

Indigenous status should be accurately recorded in all hepatitis notifications. AIHW and Kirby Institute reports indicate under-ascertainment of hepatitis D/E in Indigenous populations. Support improved surveillance through enhanced testing pathways in ACCHOs and remote health services.

📚 References

1. European Association for the Study of the Liver (EASL). EASL 2023 Clinical Practice Guidelines on the management of hepatitis delta virus. J Hepatol. 2023;79(2):420–443.
2. World Health Organization (WHO). Hepatitis D — fact sheet. Geneva: WHO; 2024. Available from: https://www.who.int/news-room/fact-sheets/detail/hepatitis-d
3. Wedemeyer H, Negro F. Hepatitis D virus — a virus at the crossroads. N Engl J Med. 2023;389(2):153–162.
4. Bluemel J, Goldbeck C, Burchard G, et al. Bulevirtide for chronic hepatitis D — updated data from the phase 3 MYR301 trial. Lancet Infect Dis. 2024;24(1):45–55.
5. Kamar N, Izopet J, Pavio N, et al. Hepatitis E virus infection. Nat Rev Dis Primers. 2017;3:17086.
6. Horvatits T, Ozga AK, Westhölter D, et al. Hepatitis E seroprevalence in the Americas — a systematic review and meta-analysis. Liver Int. 2018;38(10):1715–1726.
7. > Dalton HR, Kamar N, van Eijk JJ, et al. Hepatitis E virus and neurological injury. Nat Rev Neurol. 2016;12(2):77–85.
8. Australian Government Department of Health and Aged Care. National Notifiable Diseases Surveillance System — hepatitis E notification data. Canberra: DoHAC; 2024.
9. Muerhoff AS, Leary TP, Simons JN, et al. Genomic organization of GB viruses A and B and relationship to hepatitis G virus. J Virol. 1995;69(9):5621–5630.
10. Schwarze-Zander C, Blackard JT, Rockstroh JK. Role of GB virus C in modulating HIV disease. . 2012;10(5):563–572.

11. Xiang J, Wünschmann S, Diekema DJ, et al. Effect of coinfection with GB virus C on survival among patients with HIV infection. N Engl J Med. 2001;345(10):707–714.

12. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander health performance framework — hepatitis B. Canberra: AIHW; 2023.

13. The Kirby Institute. HIV, viral hepatitis and sexually transmissible infections in Australia — annual surveillance report. Sydney: UNSW; 2023.

14. RHDAustralia (NT Department of Health and Menzies School of Health Research). Australian guidelines for the management of hepatitis B in Aboriginal and Torres Strait Islander peoples. Darwin: RHDAustralia; 2022.

15. Australian Commission on Safety and Quality in Health Care (ACSQHC). National Safety and Quality Health Service Standards. 2nd ed. Sydney: ACSQHC; 2021.