Viral Hepatitis
Written 17th March 2020 - Last Update 27th August 2026
Viral Hepatitis
Overview — Hep A/B/C at a glance
| Hep A | Hep B | Hep C | |
|---|---|---|---|
| Acute symptoms | Most get symptoms | Most, but may be subclinical | Usually asymptomatic |
| Chronic infection rate | None | 90% if infected as an infant, 25–50% as a child, <5% as an adult | ~75% (25% spontaneously clear, usually within 6 months, up to 12) |
| Cirrhosis risk (chronic) | No (rare acute fulminant hepatitis) | ~25% over 20–40yrs if untreated | 10–20% over 30yrs |
| Transmission | Faecal-oral | Blood, sexual, household/close contact, vertical (mother-to-child, usually at birth) | Blood-to-blood; sexual/perinatal transmission uncommon |
| Cure available | Self-limiting | Suppressive antivirals (not curative) | Curative DAAs, >95% SVR |
Reinfection is always possible after clearance (natural or treated) for both HBV and HCV — clearance is not immunity.
Hepatitis A
Faecal-oral transmission, less prevalent in developed countries. Pre-icteric phase: malaise, nausea/vomiting, anorexia, fever, RUQ discomfort. Icteric phase (many patients never develop jaundice): jaundice, dark urine, pale stools, hepatomegaly ± splenomegaly. Ask about recent travel and prior immunisation.
Investigations: LFTs (↑bilirubin, ↑ALT>AST, ratio stable over time); HAV IgM (active infection); HAV IgG (past infection/immunity).
Management: self-limiting, recovery in 3–6 weeks; fulminant hepatitis rare. Rest, fat-free diet, avoid alcohol/smoking/hepatotoxic drugs, strict hand hygiene, avoid preparing food for others or sharing crockery/cutlery while infectious. Travel vaccination available (purchase, not NIP-funded for this indication).
Hepatitis B (HBV)
Epidemiology
An estimated ~79,500 people in NSW have chronic HBV, many undiagnosed — locally (Hunter New England) only ~9% are receiving care and ~4.5% receiving treatment, well below the national strategy targets (50% care, 20% treatment). Transmitted via blood, sexual contact, and mother-to-child at birth. Incubation 45–180 days; HBsAg typically detectable 1–9 weeks post-exposure (average 4 weeks). <5% of acutely infected adults develop chronic infection, but the risk is much higher with infection in infancy (90%) or childhood (25–50%) due to less mature immune responses. Infection is chronic if HBsAg remains positive >6 months.
The four phases of chronic HBV infection
| Phase | HBeAg | ALT | HBV DNA | Risk |
|---|---|---|---|---|
| 1. Immune tolerant | Positive | Normal | High (>100,000 IU/mL) | Low progression risk; typically children/young adults |
| 2. Immune clearance | Positive | Fluctuating/raised | High, fluctuating | Prolonged flares (>6–12mo) risk permanent fibrosis — an indication for treatment |
| 3. Immune control | Negative | Normal | Low (<2000 IU/mL) | Most stay here long-term |
| 4. Immune escape (“eAg-negative CHB”) | Negative | Raised, fluctuating | Moderate (>2000 IU/mL) | Up to 25% of those in immune control eventually reach this “escape” phase, usually older patients; high progression risk |
Antiviral treatment is most effective in the active phases (2 and 4) and in anyone with cirrhosis.
Who to screen (once only, absent new risk exposure — this is usually a
childhood-acquired infection)
Born in Asia/Pacific Islands/Africa/Middle East/Eastern or Southern Europe/South or Central America/Caribbean; First Nations people; MSM; current/past incarceration; HCV or HIV co-infection; chemo/immunosuppressive therapy; household or sexual contact of an HBV-positive person; people who inject drugs; abnormal LFTs; dialysis patients; pregnant women; babies of HBV-positive mothers; unvaccinated patients. Also test after high-risk exposure (needlestick, healthcare workers, sexual assault victims).
Testing and interpretation
Three simultaneously-Medicare-rebatable tests (write “?chronic hepatitis B” on the form): HBsAg, anti-HBc, anti-HBs.
| HBsAg | Anti-HBc | Anti-HBs | Meaning | Action |
|---|---|---|---|---|
| − | − | − | Susceptible | Immunise if household/HCW contact of HBV |
| − | + | + (>10) | Immune (resolved infection) | Refer if starting immunosuppression/chemo |
| − | − | + (>10) | Immune (vaccinated) | No action |
| − | + | − | Usually past infection with waned anti-HBs (>90%) | Reassure; check viral load + refer only if unexplained ↑ALT, suspected cirrhosis, or significant immunosuppression planned/occurring |
| + | + | − (± IgM anti-HBc) | Current infection (acute if IgM+/high titre; chronic or flare if IgM− /low titre) | Full staging work-up (below) |
Staging a positive HBsAg result
Further tests: HBeAg/anti-HBe, HBV DNA (quantitative — only Medicare- funded once/year if not on treatment), FBC, EUC, INR, AFP, hepatitis A serology, HCV/HIV serology. ALT thresholds: raised = >30 U/L (men), >19 U/L (women). Calculate an APRI score (AST:platelet ratio) — refer if >1.
Cirrhosis assessment: ultrasound only if cirrhosis is suspected/proven (only splenomegaly/enlarged portal vein on ultrasound is specific for cirrhosis — liver texture/shape alone is not). Liver stiffness: APRI <1.0 with no clinical concern needs no further work-up; APRI ≥1.0, or <1.0 with an increased pre-test probability (chronic liver disease signs, heavy alcohol use), warrants a Fibroscan (>12.5kPa = cirrhosis). Ultrasound-based shock-wave elastography from private radiology is less well validated than Fibroscan — very high/low readings are likely accurate, mid-range readings are of unclear significance.
Treatment thresholds and options
Refer for antiviral treatment consideration if HBsAg-positive and: HBeAg- positive with raised ALT (regardless of viral load), or HBeAg-negative with viral load >2000 IU/mL (regardless of ALT), or proven/suspected cirrhosis, or co-infected with HCV/HIV.
Antivirals: PEG-interferon alfa-2a (weekly injections, 12 months) or long-term oral entecavir or tenofovir (generally preferred — well tolerated, low resistance, suppress but don’t cure, given indefinitely). All patients with cirrhosis who are HBsAg-positive should receive entecavir or tenofovir irrespective of viral load. Prescribing requires either a specialist or a GP who has completed HBV-prescriber S100 training. Risk of acute flare if treatment is stopped without medical advice — patients still need HCC surveillance even after a good antiviral response, since risk is reduced but not eliminated.
Long-term monitoring
- Immune tolerant/control phase (normal ALT): yearly HBV DNA, LFTs, EUC, FBC.
- Immune clearance/escape phase, not on treatment: 6-monthly FBC/EUC/LFT, yearly HBV DNA.
- On treatment: per shared-care plan with the specialist.
- 2-yearly liver fibrosis assessment.
- 6-monthly HCC surveillance (ultrasound + AFP) if high risk: First Nations people >50yrs, Asian men >40yrs, Asian women >50yrs, Africans >20yrs, cirrhosis, or family history of HCC.
- Higher cirrhosis risk with: longer infection duration, age >45, high viral load, recurrent ALT flares, immunosuppression, male sex, HBeAg-positive with high viral load, co-infection (HCV/HDV/HIV), heavy alcohol (>40–50g/day), or no treatment.
Pregnancy, exposure, and prevention
Refer urgently if pregnant/planning pregnancy, to consider treatment reducing mother-to-child transmission; screen babies of positive mothers at 12 months. Post-exposure prophylaxis: unvaccinated + high-risk exposure → HBIG (within 72h) + vaccination course; vaccinated with a documented immune response needs no treatment; known non-responders may need HBIG + a booster/revaccination series — see the Australian Immunisation Handbook for the full decision table. Free vaccination (NSW Health-funded) is available for catch-up in <20yrs, First Nations people, household/sexual contacts of cases, immunosuppressed people, people with HIV/HCV, MSM, refugees, people who inject drugs, sex workers, and sexual health clinic patients (not for overseas travel). Advise alcohol reduction (abstinence if cirrhotic, otherwise <4 standard drinks on <4 days/week), smoking cessation, and avoiding herbal supplements.
Hepatitis C (HCV)
Testing
Gain informed consent (patient-requested tests don’t require disclosing a risk reason). Reflex testing — request HCV RNA automatically if HCV Ab returns positive, using a second collected tube, to avoid a repeat venepuncture visit.
Test if: increased-risk exposure (current/past injecting drug use — even once; pre-1990 blood products; unregulated tattoos/piercings; incarceration; overseas medical/dental treatment; First Nations descent; migration from a high-prevalence region; HCV-positive mother; HIV/HBV co-infection; sexual partner of an HCV-positive person, especially MSM; MSM on/eligible for PrEP); clinical or biochemical evidence of HCV (persistently deranged ALT, raised INR/bilirubin, hypoalbuminaemia, or symptoms — fatigue, nausea, headache, arthralgia, upper abdominal pain, fatty-food/alcohol intolerance; or advanced disease signs); possible exposure history; pregnancy; patient request; or needlestick/contact-tracing exposure.
Interpretation:
- Negative HCV Ab: repeat in 1–2 months if recent exposure (takes 8–11 weeks on average to seroconvert); otherwise reassure, screen annually if ongoing risk (3–6-monthly if high-risk injecting).
- Positive HCV Ab: indicates exposure (lifelong positive, not protective) — request HCV RNA to confirm current infection.
- Negative HCV RNA: if <6 weeks post-exposure, repeat in 1–2 months; if further out, active infection is unlikely — repeat once more at 3 months (2 undetectable results ≥1 month apart confirms spontaneous clearance: no treatment needed, no infectivity, normal life expectancy, but not immunity — reinfection is possible, and the patient can still be an organ donor but not a blood donor).
- Positive HCV RNA: confirms current infection. If recent exposure, recheck at ≥6 months to determine spontaneous clearance vs chronic infection; chronic HCV is confirmed at >6 months (or 2 positive results ≥6 months apart) and the patient may be suitable for curative treatment.
Pre-treatment work-up
Detailed history (duration, prior treatment, co-factors for faster fibrosis — heavy alcohol >40g/day, HIV/HBV co-infection, diabetes/obesity/metabolic syndrome, age >40, infection >20 years, male sex); examination for cirrhosis signs, BMI, waist circumference, BP. Pathology: HCV genotype (Medicare-covered, no longer required for treatment decisions — don’t delay treatment awaiting it), quantitative HCV RNA, HIV serology, hepatitis A/B serology, FBC/EUC/LFT/ INR/fasting lipids/glucose, AFP, pregnancy test. Cirrhosis assessment (upper abdominal ultrasound + liver fibrosis assessment) if feasible — if not readily available, it’s reasonable to start treatment and complete scans within 2–3 weeks.
Treatment — GP-prescribable, curative
All patients with chronic HCV should be considered for direct-acting antiviral (DAA) treatment — these can be prescribed by GPs and nurse practitioners, PBS- funded for all genotypes, cure rate >95% including in cirrhosis and prior non-responders to older protease-inhibitor regimens.
Pan-genotypic regimens suitable for GP-initiated treatment-naive patients with compensated liver disease:
- Glecaprevir + pibrentasvir (e.g. Maviret) — 8 weeks, 3 tablets once daily (non-cirrhotic or cirrhotic).
- Sofosbuvir + velpatasvir (e.g. Epclusa) — 12 weeks, 1 tablet once daily (non-cirrhotic or cirrhotic).
Sofosbuvir + velpatasvir + voxilaprevir is a third PBS-funded regimen reserved as rescue therapy for first-line failure, used in specialist care.
Refer instead of GP-initiating treatment if: suspected/confirmed cirrhosis; HBV or HIV co-infection; adherence concerns; prior anti-HCV treatment experience (prior interferon-based treatment failure does not need specialist referral); CKD stage 4/5 (sofosbuvir contraindicated — glecaprevir+pibrentasvir is safe here); pregnancy/breastfeeding (DAAs not recommended — insufficient safety data); age <18yrs (refer to paediatrics); or if the patient/GP wants specialist input. During-treatment monitoring is minimal for most patients (unlike older interferon-based regimens) — reserve extra review for adherence concerns or significant comorbidity.
Follow-up
Confirm cure (SVR): HCV RNA (qualitative) at ≥12 weeks post-treatment
(4 weeks acceptable as a compromise if the patient won’t be reachable at 12).
SVR achieved + normal LFTs + no advanced fibrosis → no further follow-up
needed (but the patient is not immune — reinfection remains possible).
SVR achieved but persistent abnormal LFTs → investigate other causes (alcohol,
medications, fatty liver, haemochromatosis, HBV, autoimmune hepatitis, coeliac
disease, Wilson’s disease, alpha-1-antitrypsin deficiency — see
abnormal-lfts.md); refer if ALT >5× ULN or no cause found. Failure to achieve
SVR → refer for retreatment consideration. Ongoing injecting risk or new
hepatic dysfunction → recheck with quantitative HCV RNA, not an antibody
test (HCV Ab stays positive lifelong after SVR).
Disclosure and transmission
Legally required disclosure: blood/sperm donation, exposure-prone healthcare procedures, some life insurance applications, ADF membership, boxing/martial arts competition. Otherwise disclosure is a personal choice. Advise safer injecting practices (needle/syringe programs, regular BBV screening) and offer hepatitis A/B vaccination to all patients with chronic HCV.