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Gastroenterology›Condition·Updated Jul 11, 2026·v1

Hepatitis C

Hepatitis C is a curable systemic infection caused by HCV, with pangenotypic DAAs achieving SVR >95% in 8-12 weeks. After cure, patients with advanced fibrosis (F3/F4) require indefinite HCC surveillance and consideration of aspirin chemoprevention. The dramatic therapeutic advance from interferon to DAAs has transformed prognosis, but residual HCC risk persists.

High Evidence597 references·10,455 words·42 min read·v1
hepatitis Cdirect-acting antiviralscirrhosishepatocellular carcinomasustained virologic responsepangenotypicFIB-4portal hypertensioncryoglobulinemiaHCV

Quick Reference

RxDrug of choiceGlecaprevir/pibrentasvir 300 mg/120 mg PO once daily for 8 weeks (non-cirrhotic) or 12 weeks (compensated cirrhosis); alternative: sofosbuvir/velpatasvir 400 mg/100 mg PO once daily for 12 weeks.
AltAlternativesSofosbuvir/velpatasvir/voxilaprevir for DAA failures; ledipasvir/sofosbuvir for genotype 1 or 4; elbasvir/grazoprevir for genotype 1 or 4 (treatment-experienced).
⊘AvoidInterferon in decompensated cirrhosis; amiodarone with sofosbuvir-containing regimens; glecaprevir/pibrentasvir in Child-Pugh C; ribavirin in pregnancy or eGFR <30.
DxTest of choiceHCV RNA by nucleic acid amplification test (NAT) to confirm active infection and monitor SVR12.
ScKey scoreFIB-4 index (age × AST / platelet × √ALT): ≤1.45 rules out advanced fibrosis; >3.25 rules in advanced fibrosis.
→When to referRefer to hepatology for decompensated cirrhosis, HCC, prior DAA failure, or complex drug interactions; refer to transplant center for HCC within Milan criteria or decompensated cirrhosis with MELD ≥15.
All patients with chronic HCV should be treated with pangenotypic DAAs for 8-12 weeks, achieving cure in >95%. After SVR, continue indefinite HCC surveillance in patients with F3/F4 fibrosis; aspirin chemoprevention may be considered in appropriate candidates.
Hepatitis C is a curable systemic infection caused by the hepatitis C virus (HCV), a single-stranded RNA virus that establishes persistent infection in 70-80% of exposed individuals. Chronic HCV is a leading cause of cirrhosis, hepatocellular carcinoma (HCC), and extrahepatic manifestations such as mixed cryoglobulinemia. The advent of direct-acting antivirals (DAAs) has transformed prognosis: pangenotypic regimens achieve sustained virologic response (SVR) rates exceeding 95% in 8-12 weeks. However, patients with advanced fibrosis (F3/F4) require indefinite surveillance for HCC and portal hypertension even after cure.

Overview and Recommendations

Background

  • •Hepatitis C virus (HCV) is a positive-sense, single-stranded RNA virus of the Flaviviridae family that infects hepatocytes via CD81, SR-BI, and tight-junction proteins. An estimated 71.1 million people are chronically infected worldwide, with 1.75 million new infections annually. Genotype 1 predominates globally (44%), followed by genotype 3 (25%) and genotype 4 (15%). Percutaneous exposure, chiefly injection drug use (60-80% seroprevalence in people who inject drugs) and unscreened blood transfusions before 1998, drives transmission.
  • •The virus evades innate immunity by cleaving MAVS and TRIF via NS3-4A protease, blunting interferon induction. Adaptive immune failure results from weak and short-lived CD4+ T-cell responses, exhausted CD8+ T cells with upregulated PD-1, and expanded regulatory T cells. This leads to persistent infection in 70-80% of acutely infected individuals, with chronic necroinflammation activating hepatic stellate cells and driving progressive fibrosis.
  • •Chronic HCV is a leading cause of cirrhosis (27% of cases worldwide) and HCC (25% of cases). Untreated, the annual rates of decompensation, HCC, and liver-related death in compensated cirrhosis are 6.37%, 3.36%, and 4.58%, respectively. Extrahepatic manifestations include mixed cryoglobulinemia vasculitis (7.4% gastrointestinal involvement), B-cell non-Hodgkin lymphoma (OR 2.19), insulin resistance, and porphyria cutanea tarda.
  • •The treatment paradigm has evolved from interferon monotherapy (SVR <10%) to pegylated interferon plus ribavirin (SVR 40-80%) and now to all-oral pangenotypic DAAs such as glecaprevir/pibrentasvir and sofosbuvir/velpatasvir, which achieve SVR >95% in 8-12 weeks. This revolution represents one of the most dramatic therapeutic advances in modern medicine, but residual HCC risk persists after cure in patients with advanced fibrosis.

Evaluation

  • •Suspect HCV in any patient with elevated liver enzymes, unexplained fatigue, or risk factors such as injection drug use (even remote), blood transfusion before 1998, hemodialysis, or HIV coinfection. Extrahepatic clues, palpable purpura, arthralgias, peripheral neuropathy, or blistering skin lesions (porphyria cutanea tarda), should prompt testing.
  • •Screen with anti-HCV antibody; a positive result must be confirmed by quantitative HCV RNA (nucleic acid amplification testing) to diagnose active infection. Reflexive testing (automatic HCV RNA on antibody-positive samples) is now standard. HCV core antigen is a less expensive alternative but less sensitive early in therapy.
  • •Assess genotype only if pangenotypic DAAs are unavailable or if retreatment is needed after virologic failure; genotype determination is no longer mandatory with first-line pangenotypic regimens.
  • •Stage liver fibrosis using noninvasive tools: calculate FIB-4 (age × AST / platelet × √ALT). A FIB-4 ≤1.45 rules out advanced fibrosis (F3-F4) with high sensitivity; >3.25 rules in advanced fibrosis. For indeterminate results, perform transient elastography (FibroScan). A liver stiffness measurement (LSM) ≥12.5 kPa confirms cirrhosis; LSM ≥25 kPa rules in clinically significant portal hypertension (CSPH).
  • •In patients with cirrhosis or compensated advanced chronic liver disease (cACLD), apply Baveno VII criteria (LSM ≤15 kPa plus platelets ≥150 × 10⁹/L) to identify those with <5% risk of high-risk varices, allowing safe deferral of screening esophagogastroduodenoscopy (EGD). Otherwise, perform EGD to screen for varices.
  • •Initiate hepatocellular carcinoma (HCC) surveillance with semiannual ultrasound plus α-fetoprotein (AFP) in all patients with cirrhosis (F4) or advanced fibrosis (F3). Lowering the AFP threshold to ≥10 ng/mL increases sensitivity without sacrificing specificity. Surveillance should continue indefinitely after SVR, as HCC risk remains above the cost-effectiveness threshold for at least 6 years.
  • •Also consider screening for extrahepatic manifestations: check for cryoglobulins if vasculitic symptoms are present, assess for diabetes with oral glucose tolerance test if insulin resistance is suspected, and evaluate for B-cell lymphoma if unexplained lymphadenopathy or cytopenias occur.

Management

  • •Initiate direct-acting antiviral (DAA) therapy for all patients with chronic HCV (detectable HCV RNA >6 months), regardless of fibrosis stage, unless life expectancy is limited. Treatment is urgent in acute hepatitis C and decompensated cirrhosis.
  • •First-line pangenotypic regimen: glecaprevir/pibrentasvir 300 mg/120 mg (3 tablets) once daily for 8 weeks in non-cirrhotic, treatment-naïve patients; extend to 12 weeks for compensated cirrhosis. Alternative: sofosbuvir/velpatasvir 400 mg/100 mg once daily for 12 weeks for all genotypes and stages.
  • •For decompensated cirrhosis (Child-Pugh B/C), use sofosbuvir/velpatasvir 400 mg/100 mg once daily plus ribavirin (weight-based: 1000-1200 mg/day divided BID) for 12 weeks. This achieves SVR12 of 94% and improves Child-Pugh class in 49% of patients by 3 years.
  • •Monitor HCV RNA at baseline, week 4, end of treatment, and 12 weeks post-treatment (SVR12). SVR12 is considered cure. For ribavirin-containing regimens, check hemoglobin weekly for the first month, then monthly.
  • •After SVR, patients with F3/F4 fibrosis require lifelong HCC surveillance with ultrasound plus AFP every 6 months. Recompensation occurs in ~25% of decompensated patients, but HCC risk persists (2.9% de novo rate). Continue variceal screening if cirrhosis persists.
  • •Avoid interferon-based regimens in decompensated cirrhosis or severe psychiatric illness. Do not co-administer amiodarone with sofosbuvir-containing regimens (risk of life-threatening bradycardia). Avoid glecaprevir/pibrentasvir in Child-Pugh C cirrhosis. Do not use ribavirin in pregnancy (teratogenic) or in patients with hemoglobin <10 g/dL without erythropoiesis support.
  • •For virologic failure (relapse or breakthrough), check for resistance-associated substitutions (RASs) and retreat with sofosbuvir/velpatasvir/voxilaprevir 400 mg/100 mg/100 mg once daily for 12 weeks (SVR 88.6% after prior DAA failure).
  • •In special populations: HIV coinfection, use standard DAA regimens; check drug-drug interactions with antiretrovirals. Chronic kidney disease (eGFR <30), glecaprevir/pibrentasvir is preferred (no dose adjustment). Post-liver transplant, individualize DAA regimen; monitor calcineurin inhibitor levels. Pediatrics, DAAs approved for age ≥3 years, weight-based dosing.
  • •Consider chemoprevention: aspirin ≤160 mg daily reduces HCC incidence (HR 0.69) in patients with cirrhosis, with a small increase in gastrointestinal bleeding risk (10-year risk 7.8% vs 6.9%). Coffee consumption is associated with a 40% reduction in HCC risk.

Board Review — High Yield

  • •Sustained virologic response (SVR12), undetectable HCV RNA 12 weeks after treatment completion; defines cure.
  • •Pangenotypic DAA regimens, glecaprevir/pibrentasvir and sofosbuvir/velpatasvir cover all genotypes 1-6 without need for genotype testing.
  • •Baveno VII criteria, LSM ≤15 kPa + platelets ≥150 × 10⁹/L rules out CSPH, allowing safe deferral of EGD.
  • •FIB-4 >3.25, rules in advanced fibrosis (F3-F4); associated with increased HCC risk after SVR.
  • •Decompensated cirrhosis, treat with sofosbuvir/velpatasvir + ribavirin for 12 weeks; recompensation occurs in ~25%.
  • •HCC surveillance, semiannual ultrasound + AFP indefinitely in F3/F4; AFP threshold ≥10 ng/mL improves sensitivity.
  • •Aspirin chemoprevention, ≤160 mg daily reduces HCC risk by 31% in cirrhosis; small increase in GI bleeding.
  • •Extrahepatic manifestations, mixed cryoglobulinemia (7.4% GI vasculitis), B-cell NHL (OR 2.19), porphyria cutanea tarda.
  • •HIV coinfection, DAA regimens are safe and effective; check ART interactions (e.g., efavirenz reduces ledipasvir levels).
  • •Chronic kidney disease, glecaprevir/pibrentasvir is preferred for eGFR <30; no dose adjustment needed.

Deep Dive — Evidence Details

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