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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- HCV is an RNA flavivirus transmitted primarily via blood (IVDU is commonest route in UK). NOT sexually transmitted efficiently
- Acute infection usually asymptomatic; ~75% develop chronic infection (unlike HBV where most adults clear it)
- Screen with anti-HCV antibody; confirm active infection with HCV RNA PCR
- CURATIVE treatment: direct-acting antivirals (DAAs) — e.g. sofosbuvir/velpatasvir (Epclusa) for 12 weeks = >95% SVR (cure)
- Post-treatment: confirm sustained virological response (SVR) at 12 weeks. If cirrhotic, continue 6-monthly HCC surveillance lifelong
Overview
Hepatitis C virus (HCV) is a single-stranded RNA flavivirus with 6 major genotypes. It is primarily transmitted via the blood-borne route — the most common mode in the UK is injecting drug use (past or current), though historical blood transfusion (pre-1991 screening) and needlestick injuries are also significant. Unlike HBV, most patients (75%) fail to clear acute HCV and develop chronic infection, which silently progresses over 20–30 years towards fibrosis, cirrhosis, and HCC. The advent of direct-acting antivirals (DAAs) has revolutionised management, achieving cure rates >95% with short oral regimens.
Epidemiology
Approximately 120,000 people in the UK have chronic HCV, with an estimated 40,000 undiagnosed. The UK has committed to HCV elimination by 2030 (WHO target). Genotype 1 is most common in the UK (~45%) followed by genotype 3 (~35%). Incidence is declining due to harm reduction (needle exchanges, opioid substitution) and treatment-as-prevention strategies. HCV accounts for approximately 25% of UK liver transplant waiting lists.
Clinical Features
Symptoms
Acute HCV: ~80% asymptomatic. If symptomatic: malaise, anorexia, nausea, jaundice (rare)
Chronic HCV: often asymptomatic for decades — "silent epidemic"
Fatigue (most common symptom in chronic HCV)
Arthralgia, myalgia
Features of decompensated cirrhosis (late presentation)
Signs
Usually no abnormal signs in early chronic infection
Hepatomegaly (may be tender)
Signs of chronic liver disease/cirrhosis in advanced cases
Cryoglobulinaemia: palpable purpura, arthralgia, renal impairment (extrahepatic — type II mixed cryoglobulinaemia)
Porphyria cutanea tarda (skin blistering on sun-exposed areas)
Investigations
First-line
Anti-HCV antibodyScreening test — indicates exposure (past or current). Positive does NOT distinguish active from cleared infection
HCV RNA PCRConfirms active (viraemic) infection if anti-HCV positive. Quantitative viral load and genotype guide treatment
Second-line
HCV genotypeGuides treatment regimen choice (though pan-genotypic DAAs now available)
FibroScan (transient elastography)Non-invasive fibrosis assessment — determines urgency of treatment and need for HCC surveillance
LFTs, FBC, U&Es, coagulationBaseline liver function, platelet count (low in cirrhosis/portal hypertension)
Specialist
Screen for co-infectionsHBV (HBsAg), HIV, hepatitis A immunity — co-infection accelerates progression
HCC surveillance6-monthly USS ± AFP if cirrhosis present — continue even after viral cure (SVR)
1
Direct-acting antiviral (DAA) therapy
- All patients with chronic HCV should be offered treatment regardless of fibrosis stage
- Pan-genotypic regimens: sofosbuvir/velpatasvir (Epclusa) 12 weeks — first-line for most patients
- Glecaprevir/pibrentasvir (Maviret) 8–12 weeks — alternative pan-genotypic option
- Cure rate (SVR12) >95% across all genotypes with modern DAAs
- No need for interferon in current treatment paradigms
2
Monitoring and follow-up
- Check HCV RNA at 12 weeks post-treatment completion — undetectable = SVR (cure)
- If cirrhotic: continue 6-monthly HCC surveillance USS lifelong (even after SVR — residual HCC risk persists)
- Monitor for HBV reactivation during and after DAA therapy (if HBsAg positive or anti-HBc positive)
3
Public health measures
- Notifiable disease — notify local health protection team
- Harm reduction: needle exchange programmes, opioid substitution therapy
- Screen high-risk groups: PWID, prisoners, HIV-positive MSM, migrants from endemic countries, recipients of blood products pre-1991
- Treatment-as-prevention: curing infected individuals reduces onward transmission
- No vaccine currently available for HCV
Complications
- Cirrhosis: Develops in 20–30% of chronic HCV over 20–30 years (accelerated by alcohol, HBV co-infection, obesity)
- Hepatocellular carcinoma: 1–5% annual risk in HCV cirrhosis. Continue surveillance even post-SVR
- Cryoglobulinaemia: Type II mixed — palpable purpura, arthralgia, membranoproliferative GN. Resolves with HCV cure
- Non-Hodgkin lymphoma: HCV is associated with B-cell NHL (splenic marginal zone lymphoma)
- Porphyria cutanea tarda: Skin blistering on sun-exposed areas
UKMLA Exam Tips
- 1Anti-HCV positive + HCV RNA positive = ACTIVE infection. Anti-HCV positive + RNA negative = past/cleared infection
- 2~75% of acute HCV becomes chronic (opposite to HBV where >95% of adults clear it)
- 3DAAs have >95% cure rate in 8–12 weeks — HCV is now a CURABLE disease
- 4No HCV vaccine exists (unlike HBV) — key differentiator
- 5HCC surveillance continues LIFELONG in cirrhotic patients even after successful cure
- 6IVDU is the commonest transmission route in the UK — always screen PWID
- 7HCV genotype 3 is associated with more rapid fibrosis progression and hepatic steatosis
practicetest your knowledge on hepatitis cApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — gastroenterology and beyond.
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