In New Zealand, hepatitis C is managed by gastroenterologists. Hepatitis C is a blood-borne viral infection of the liver caused by hepatitis C virus (HCV), an RNA virus that establishes chronic infection in 55-85% of newly infected adults and slowly damages the liver over decades. WHO estimates 50 million people live with chronic HCV globally, with around 1 million new infections and 242,000 deaths each year from cirrhosis and hepatocellular carcinoma.
Hepatitis C (ICD-10: B17.1 acute, B18.2 chronic) is an infection of hepatocytes caused by hepatitis C virus (HCV), a small enveloped single-stranded positive-sense RNA virus in the Flaviviridae family (Hepacivirus genus). HCV has six major genotypes (1-6) and over 80 subtypes, with regional clustering: genotype 1 (1a and 1b) dominates in North America, Europe, and Japan; genotype 2 in West Africa and Mediterranean; genotype 3 in India and Southeast Asia; genotype 4 in Egypt and the Middle East; genotype 5 in South Africa; and genotype 6 in Southeast Asia. The virus replicates in hepatocytes via an error-prone RNA-dependent RNA polymerase, producing extensive sequence diversity (quasispecies) that helps it evade host immunity and explains the lack of an effective vaccine. Acute HCV infection (lasting up to 6 months) is asymptomatic in roughly 70-80% of adults; the minority who develop symptomatic acute hepatitis have jaundice, fatigue, and right-upper-quadrant pain.
The key symptoms of Hepatitis C are: Most acute hepatitis C infections (70-80%) produce no symptoms., When symptomatic, acute hepatitis C causes 2-12 weeks of fatigue, anorexia, nausea, right-upper-quadrant abdominal pain, dark urine, pale stools, and jaundice 2-26 weeks after exposure., Most chronic HCV is asymptomatic for years to decades and detected on routine blood tests or by screening., Persistent fatigue, malaise, and low energy out of proportion to other findings — common subjective complaint in chronic HCV., Right-upper-quadrant abdominal discomfort, mild nausea, or itching in long-standing disease., Joint pain, muscle aches, dry eyes, dry mouth, and small-vessel vasculitic skin lesions (palpable purpura) in HCV-associated mixed cryoglobulinemia., Sun-induced blistering, fragile skin, and hyperpigmentation in HCV-related porphyria cutanea tarda..
Diagnosis follows a two-step algorithm. The first test is anti-HCV antibody by enzyme immunoassay; if positive, HCV RNA by reverse-transcription PCR confirms active infection (anti-HCV positive with negative HCV RNA indicates spontaneously cleared past infection or false-positive antibody). HCV RNA quantitation provides baseline viral load (not strongly predictive of disease progression but used to assess treatment response in some protocols). Genotype testing was historically required to choose the right DAA regimen and treatment duration; with widespread pan-genotypic regimens, genotype testing is no longer essential for most patients in most countries, but remains useful in cirrhotics, retreatment, and resource-limited regions using genotype-specific regimens. Once HCV infection is confirmed, staging of fibrosis is critical because patients with advanced fibrosis (F3-F4) require more careful regimen selection, lifelong HCC surveillance, and management of portal hypertension. Non-invasive fibrosis assessment is now standard: simple scores (FIB-4 above 3.25 strongly suggests advanced fibrosis; APRI above 2.0 suggests cirrhosis) and transient elastography (FibroScan: liver stiffness above 12.5 kPa highly suggestive of cirrhosis in HCV) have largely replaced liver biopsy. All HCV-positive patients should also be screened for HIV, hepatitis B (HBsAg, anti-HBs, anti-HBc) to identify coinfection and prevent reactivation during DAA therapy, and abdominal ultrasound to detect HCC. Patients with cirrhosis or advanced fibrosis need 6-monthly abdominal ultrasound plus alpha-fetoprotein for life. Patients with extra-hepatic manifestations (cryoglobulinemia, glomerulonephritis, lymphoma) require additional workup and treatment beyond DAAs.
The prognosis of hepatitis C has been transformed by direct-acting antivirals. Modern pan-genotypic DAA regimens achieve SVR12 (cure) in over 95% of treated patients, regardless of genotype, prior treatment exposure, HIV coinfection, or compensated cirrhosis. Cure substantially reduces all-cause mortality (70-80%), liver-related mortality (over 80%), HCC risk (50-70% reduction but not abolished — surveillance continues for cirrhotic patients), and largely resolves extra-hepatic manifestations including cryoglobulinemic vasculitis, glomerulonephritis, and HCV-associated lymphoma. Liver fibrosis (including early cirrhosis) can regress over years after cure. Decompensated cirrhosis improves in many patients after cure but established complications often persist. Untreated chronic HCV progresses to cirrhosis in 15-30% over 20-30 years, with an annual HCC risk of 1-4% once cirrhosis is established. Reinfection after cure is possible because no protective immunity develops; reinfection rates are highest among people who continue to inject drugs (3-30 per 100 person-years) and HIV-positive MSM. Periodic re-testing and harm reduction reduce reinfection risk. The WHO 2030 elimination targets (90% reduction in new infections, 65% reduction in mortality) are technically achievable with widespread DAA access, comprehensive screening, and integrated harm reduction; Egypt, Iceland, Australia, Georgia, and several other countries have already met or are on track to meet milestone targets.
Most uncomplicated HCV can now be treated by trained primary care providers and nurse practitioners with protocol-driven regimens. Specialist hepatology or infectious disease referral is recommended for cirrhosis (especially decompensated), HIV-HCV coinfection, prior treatment failure, renal impairment, transplant candidacy, and extra-hepatic manifestations.
Find specialists →Acute HCV: 70-80% of acute infections are asymptomatic; symptomatic disease resolves over 6-12 weeks; spontaneous clearance occurs within 6 months in 15-45%. DAA therapy: most patients become HCV RNA undetectable within 4 weeks of starting treatment; SVR12 confirms cure 12 weeks after end of treatment. Fibrosis regression: gradual over 1-5 years after cure; cirrhosis can regress histologically in many patients. HCC surveillance: continues every 6 months for life in patients with cirrhosis even after cure.
Regular moderate aerobic exercise (150 minutes per week) and resistance training reduce hepatic steatosis, support weight management, and improve quality of life. Vigorous exercise is safe in compensated HCV. Avoid contact sports during severe thrombocytopenia or active variceal disease.
For uncomplicated cases, choose a primary care provider, addiction-medicine clinician, or infectious disease specialist familiar with the AASLD/IDSA HCV Guidance. For cirrhosis, prior treatment failure, or HIV coinfection, see a hepatologist with access to FibroScan, HCC surveillance imaging, and full DAA formulary. Transplant evaluation requires a designated liver transplant centre.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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