viral hepatitis

HBV is the highest-yield virus for Canadian IM exams — know the serology table cold, CASL 2025 treatment indications, and HCC surveillance criteria. HCV is now curable with 8–12 weeks of pan-genotypic DAAs; the main exam angle is who still needs surveillance after cure. HAV is self-limited; know PEP indications. HDV reflex testing is now routine for all HBsAg(+) patients.

hepatitis A

Faecal-oral transmission; self-limited, no chronicity
Diagnosis: anti-HAV IgM
PEP indications: household contacts, childcare contacts, co-workers/clients of infected food handlers
No specific treatment; supportive care

hepatitis B

serology patterns

pattern	HBsAg	anti-HBs	anti-HBc IgM	anti-HBc IgG	HBV DNA
acute infection	+	−	+	−	+
window period	−	−	+	±	±
resolved infection	−	+	−	+	−
vaccination	−	+	−	−	−
chronic infection	+ (≥6 mo)	−	−	+	±

HDV co-testing

HDV reflex testing is now routine for all HBsAg(+) patients. HDV requires HBsAg for replication — co-infection accelerates progression to cirrhosis and increases HCC risk. Test with anti-HDV Ab; if positive, confirm with HDV RNA.

treatment indications (CASL 2025)

Cirrhosis or HCC
Planned immunosuppressive therapy or extrahepatic manifestations (PAN, membranous nephropathy, cryoglobulinaemia)
HBV DNA >2000 IU/mL + elevated ALT persisting 3–6 months (regardless of HBeAg status)
HBV DNA >2000 IU/mL + any of: age ≥40, liver stiffness ≥7 kPa (≥F2 fibrosis), family history of HCC or cirrhosis
Pregnancy: HBV DNA >200 000 IU/mL → initiate tenofovir (TDF or TAF) by 2nd trimester to prevent mother-to-child transmission. Newborn receives HBIG + vaccine within 12 hours

first-line medications

agent	notes
tenofovir alafenamide (TAF)	preferred — lower bone and renal toxicity than TDF
tenofovir disoproxil (TDF)	effective but can cause Fanconi syndrome / type 2 RTA; preferred in pregnancy (more safety data)
entecavir (ETV)	alternative first-line; avoid if prior lamivudine resistance

All are nucleos(t)ide analogues given indefinitely — functional cure (HBsAg loss) occurs in <10%. Finite therapy may be considered in HBeAg-positive patients who achieve HBeAg seroconversion with undetectable DNA, consolidated for ≥12 months.

immunosuppression and HBV reactivation

Screen all patients starting immunosuppressive therapy with HBsAg + anti-HBc. Even resolved infection (HBsAg−, anti-HBc+) can reactivate with anti-CD20 agents (rituximab), high-dose steroids, or chemotherapy. Pre-emptive antiviral therapy prevents fulminant reactivation hepatitis.

HCC surveillance (q6 months US + AFP)

indication	threshold
cirrhosis (any aetiology)	all patients
African ancestry	age ≥30 (even without cirrhosis)
Asian males	age ≥40
Asian females	age ≥50
family history of HCC	start at age 40 or 10 years before youngest index case

hepatitis C

diagnosis and screening

Diagnosis: anti-HCV Ab → if positive, confirm active viraemia with HCV RNA
Screening: universal one-time screening for adults ≥18 (AASLD) or birth cohort 1945–1975 (CASL)
Anti-HCV Ab remains positive lifelong even after cure — only HCV RNA distinguishes active from resolved infection

treatment

Pan-genotypic direct-acting antivirals (DAAs):

regimen	duration	notes
sofosbuvir/velpatasvir (Epclusa)	12 weeks	all genotypes; can use in decompensated cirrhosis
glecaprevir/pibrentasvir (Maviret)	8 weeks	all genotypes; shorter course

decompensated cirrhosis (Child-Pugh B/C)

Maviret is contraindicated — contains a protease inhibitor with hepatotoxic risk in decompensated disease. Use Epclusa ± ribavirin only.

cure and post-treatment surveillance

SVR12 = undetectable HCV RNA 12 weeks post-treatment → defines virological cure
Cure rates exceed 95% across genotypes with current DAAs
Cirrhotic patients require lifelong HCC surveillance (q6 months US + AFP) even after achieving SVR12 — fibrosis regression is slow and HCC risk persists, particularly if advanced fibrosis/cirrhosis was present before treatment

hepatitis E

Brief mention for completeness — usually self-limited and faecal-oral like HAV. Two exam-relevant points:

can cause chronic hepatitis in immunosuppressed patients (solid organ transplant recipients) → treat with ribavirin
risk of fulminant hepatic failure in pregnancy (up to 25% mortality in 3rd trimester)

common traps

Isolated anti-HBc positive — does not mean “immune.” Could be window period, remote resolved infection with waned anti-HBs, or occult HBV. Check HBV DNA before immunosuppression.
HCV Ab positive, RNA negative — this is cured or spontaneously cleared infection, not active disease. No treatment needed, but document SVR if post-treatment.
Stopping HBV antivirals prematurely — risk of severe reactivation flare, including acute liver failure. Indefinite therapy is the default.
Forgetting HCC surveillance after HCV cure — SVR12 eliminates the virus, not the fibrosis-driven cancer risk.

related: approach to elevated liver enzymes · cirrhosis · decompensated cirrhosis · hepatocellular carcinoma · hereditary hemochromatosis