Hepatitis C

• Hepatitis C is an infection of the liver caused by the hepatitis C virus (HCV), a small RNA virus in the flavivirus family. It is spread by contact with infected blood, not by casual contact.
• About 47 million people worldwide have chronic hepatitis C, with about 0.9 million new infections each year. ^[1] Around 70% of acutely infected people develop chronic infection. Estimates of cirrhosis risk differ by guideline: WHO estimates 15% to 30% within 20 years, and CDC estimates 5% to 25% over 10 to 20 years. ^{[1] [3]}
• Most new infections are silent: acute hepatitis C is usually symptomless. It is found by screening, or years later when liver damage has developed.
• The cure is one of modern medicine's great successes: a short course (8 to 12 weeks) of oral direct-acting antivirals (DAAs) cures more than 95% of people. ^{[1] [2]}
• There is no vaccine and no post-exposure prophylaxis. Prevention is therefore about avoiding blood contact, testing and treating infection, and harm reduction. ^{[1] [3] [7]}

By the end of this page you should be able to:

1. Explain how HCV is transmitted and why it is a global public-health problem, especially among people who inject drugs.
2. Describe the natural history from acute infection through chronic hepatitis, cirrhosis and hepatocellular carcinoma, including the main extrahepatic manifestations.
3. State who should be screened and how the two-step diagnosis (anti-HCV antibody, then HCV RNA) works.
4. Choose and monitor an appropriate oral DAA regimen for treatment-naive adults with and without cirrhosis, and state typical durations.
5. Recognise the situations that need specialist care: decompensated cirrhosis, HIV or hepatitis B coinfection, renal impairment, pregnancy, children, and treatment failure.
6. Explain why cirrhosis still needs hepatocellular carcinoma surveillance after cure, and what follow-up and harm reduction are needed.

Hepatitis C is best understood as a spectrum. At one end is an acute infection that usually causes no symptoms. At the other end is chronic disease, which may be silent for 20 years or more before cirrhosis or liver cancer declares itself. The arrival of curative oral drug therapy has moved the aim from control to elimination of hepatitis C as a public health problem. ^{[1] [2]}

This page covers HCV infection in adults in detail, and the modifications needed for children, pregnancy and renal impairment. It does not cover the rare acute liver failure of hepatitis C, which is exceptional.

Hepatitis C occurs in every region of the world. An estimated 47 million people have chronic hepatitis C, with about 0.9 million new infections each year, and about 239,000 people died from hepatitis C in 2024, mostly from cirrhosis and hepatocellular carcinoma. ^[1] The highest burden is in the Eastern Mediterranean region, with 12 million people chronically infected; the African region carries about 8 million, South-East Asia and Europe about 9 million each, the Western Pacific about 7 million, and the Americas about 5 million. ^[1]

Egypt deserves special mention. Egypt historically had one of the highest hepatitis C prevalences in the world, driven by past mass treatment campaigns using parenteral antischistosomal drugs. Aggressive population screening and treatment using cheap generic direct-acting antivirals have become a showcase elimination programme, and prevalence has fallen dramatically as a result. ^[1]

In the United States about 2.4 million people live with current HCV infection, and incidence has risen sharply in younger adults who inject drugs. ^[3] Acute infection is greatest in people aged 20 to 29 years, and only a few of the actual cases are reported in any year. ^[3]

• Age. New infections in many countries now occur mainly in young adults (20 to 39 years) who inject drugs, while older birth cohorts still carry most chronic disease. ^{[2] [3]}
• Sex. Overall infection is slightly more common in men. ^[3]
• Geography. The Eastern Mediterranean region carries the largest share of chronic infection; the African region carries a large share, including a substantial, often undiagnosed, burden in sub-Saharan Africa. ^[1]

Hepatitis C is a blood-borne virus. The main routes are:

• Injection drug use. Sharing needles, syringes, water, cookers, filters or other preparation equipment is the dominant mode of transmission in high-income countries. ^{[3] [7]}
• Healthcare exposure. Reuse or inadequate sterilisation of medical equipment, especially syringes and needles, and unsafe invasive procedures. ^{[1] [3]} Occupational needlestick and other sharps injuries also transmit HCV: CDC estimates the risk is about 0.2% with recent data, while older literature cited by CDC averages about 1.8% (range 0 to 7%) per percutaneous exposure, so the reported span is 0.2% to 1.8% (recent versus older estimates). Mucocutaneous exposure is effectively zero. ^[7]
• Blood products before screening. Before universal testing of the blood supply (1992 in the United States), transfusion was a common route. Receipt of blood or blood components before July 1992, organ transplant before July 1992, or clotting factor concentrates produced before 1987 still identifies people at risk. ^{[2] [3]}
• Vertical (mother to child). Occurs in about 5% to 6% of infants born to mothers with detectable HCV RNA, and about twice as often when the mother also has HIV. ^{[2] [3]}
• Sexual transmission. Uncommon in the general population, but important among men who have sex with men, particularly those with HIV, and in people with multiple partners where blood exposure can occur. ^{[1] [2]}
• Tattoos and piercing in unregulated settings.
• Uncommon relative routes: sharing razors or toothbrushes that carry blood, drug use by the intranasal route, and birth to an infected mother. ^[3]

Hepatitis C is not spread by breast milk, food, water, or casual contact such as hugging, kissing or sharing food or drink. ^[1]

Acute infection is usually silent. When symptoms occur, they are mild and non-specific (fatigue, anorexia, abdominal discomfort, sometimes jaundice), 2 to 12 weeks after exposure. ^[3] Fulminant liver failure is rare. ^[3]

The key fact for prognosis is spontaneous clearance: around 30% of people clear the virus within 6 months, while the remaining 70% develop chronic infection. ^{[1] [3]} One recent series estimates clearance may be as high as 46%, and is lower with HIV coinfection. ^[3] People who clear acute infection make HCV antibodies but no RNA, and they remain at risk of reinfection. ^[2]

Chronic hepatitis C is usually silent for 20 years or more. Symptoms, when they appear, come from cirrhosis or cancer rather than from hepatitis itself. Estimates of cirrhosis risk differ between guidelines: WHO estimates that 15% to 30% of people with chronic HCV develop cirrhosis within 20 years, whereas CDC estimates 5% to 25% over 10 to 20 years. ^{[1] [3]} Once cirrhosis is present, hepatocellular carcinoma develops at roughly 1% to 4% per year. ^[3]

Progression is faster in men, in people over 50 years, with alcohol use, non-alcoholic fatty liver disease, hepatitis B or HIV coinfection, and immunosuppression. ^[3] Alcohol matters plainly: there is no safe level of alcohol for a person with chronic hepatitis C. ^[2]

Hepatitis C is a systemic disease as well as a liver disease. Extrahepatic problems are common and can dominate the clinical picture. ^[5]

Cryoglobulinaemia deserves emphasis. In mixed cryoglobulinaemia, cold-precipitable immune complexes containing HCV antigen deposit in small vessels, producing purpura, arthralgia or arthritis, peripheral neuropathy (often mononeuritis multiplex) and membranoproliferative glomerulonephritis. Antiviral treatment that clears HCV commonly improves these manifestations. ^{[2] [5] [6]}

HCV is acquired, not inherited. Risk is driven by blood exposure, not by host genetics alone. The risk groups that should prompt testing are:

• Behaviours. Current or past injection drug use, even once; intranasal illicit drug use; men who have sex with men. ^[2]
• Exposures. Long-term haemodialysis; percutaneous or parenteral exposures in unregulated settings (tattoos, piercings); healthcare, emergency and public safety workers after needlestick, sharps or mucosal exposure to HCV-infected blood; children born to HCV-infected mothers; people who have ever been incarcerated; prior recipients of a transfusion (before July 1992) or organ transplant (before July 1992), or of clotting factors produced before 1987; people who shared blood-contaminated personal items. ^{[2] [3]}
• Conditions. HIV infection; people starting HIV pre-exposure prophylaxis; unexplained chronic liver disease or persistently abnormal alanine aminotransferase; solid organ donors and recipients. ^[2]
• Other vulnerabilities. Birth during 1945 to 1965 was the traditional birth-cohort risk group in the United States; sexual partners of people with chronic HCV; infants born to mothers with HCV. ^[3]

HCV is an RNA virus with a high mutation rate that helps it evade immunity. ^[3] Several points explain the clinical picture:

1. Hepatocyte tropism. HCV infects and replicates in hepatocytes, causing continuous immune-mediated inflammation. ^[5]
2. Acute persistence. In most people initial immune responses fail to clear the virus; roughly 70% go on to chronic infection. ^[1]
3. Fibrosis accumulation. Repeated necroinflammation activates hepatic stellate cells; collagen is laid down faster than it is cleared. Fibrosis may be accelerated by alcohol, metabolic disease, HBV or HIV coinfection and immunosuppression. ^[3]
4. Systemic immune activation. HCV-driven immune complex formation (notably in mixed cryoglobulinaemia) explains renal, skin and neurological disease. ^[6]
5. Oncogenesis. Long-standing cirrhosis and viral proteins promote hepatocellular carcinoma; risk falls but does not disappear with viral clearance. ^[2]

As noted, usually silent. Less often there is a mild hepatitis with fatigue, anorexia, nausea, abdominal pain and, in 20% to 30% of symptomatic patients, jaundice. ^[3] The average incubation period is 2 to 12 weeks (range 2 to 26 weeks). ^[3]

Chronic hepatitis C is symptomless in most people. When found, it is often through screening, through an incidental abnormal alanine aminotransferase, or when complications appear. Non-specific symptoms (fatigue, brain fog) are reported but are unreliable. ^[5]

On examination in early disease there may be nothing to find. With cirrhosis, signs of portal hypertension and liver failure appear (ascites, varices, encephalopathy, splenomegaly), and there may be stigmata of chronic liver disease. ^{[2] [3]}

The main alternatives to consider are other causes of chronic liver disease and hepatitis. The difference is made by virology plus clinical context.

The diagnosis is made in two steps. Anti-HCV antibody testing finds people ever infected; HCV RNA confirms current infection. ^{[2] [3]}

Use an HCV RNA assay with a lower limit of detection of at least 25 IU per mL. ^[2] Quantitative HCV RNA before treatment documents the baseline viremia; ^[2] HCV genotype testing is no longer universally required now that pangenotypic regimens dominate, but it is still done for anyone with a prior treatment failure, and for people with compensated cirrhosis treated with sofosbuvir/velpatasvir, where it determines whether baseline resistance testing is needed. ^[2]

Baseline assessment in every person with active infection should include:

• Severity of liver disease: liver function tests, platelet count, international normalised ratio, albumin, bilirubin; noninvasive fibrosis assessment; abdominal ultrasound looking at liver nodularity, spleen size and ascites. ^[2]
• Coinfections: hepatitis B surface antigen and HIV antigen/antibody test. ^[2]
• Other causes of liver disease: alcohol use, drugs, metabolic risk. ^[2]
• Vaccination: hepatitis A and hepatitis B for all susceptible people, and pneumococcal vaccination for people with cirrhosis. ^[2]
• Counselling and harm reduction: alcohol cessation (there is no safe level of alcohol in chronic hepatitis C), needle and equipment safety, condom use where appropriate, not donating blood or semen. ^[2]

Fibrosis is staged mainly with noninvasive tests rather than liver biopsy, which is now rarely needed. ^[2]

• Serum marker panels: FIB-4 score and AST-to-platelet ratio index (APRI) are the simplest. In the AASLD-IDSA simplified pathway a FIB-4 score above 3.25 counts as evidence of cirrhosis. ^[2]
• Transient elastography (for example FibroScan): liver stiffness reflects fibrosis; stiffness above about 12.5 kPa indicates cirrhosis in the simplified pathway. ^[2]
• Imaging and blood tests: nodular liver, splenomegaly, platelet count below 150,000 per mm3, bilirubin, albumin, INR all suggest advanced fibrosis or cirrhosis. ^[2]

A liver biopsy is reserved for situations where another cause of liver disease is suspected or results are discordant.

Everyone with active HCV infection should receive advice to protect their liver and prevent transmission. Alcohol should be avoided completely. ^[2] Hepatotoxic drugs are best avoided (for example excess paracetamol/acetaminophen above 2 g per day, and certain herbal supplements), and non-steroidal anti-inflammatory drugs avoided in people with cirrhosis. ^[2] Ongoing alcohol use is not a contraindication to antiviral treatment. ^[2]

Education covers avoiding sharing toothbrushes, razors, nail clippers and drug-preparation equipment, covering bleeding wounds, cleaning blood spills with a dilution of 1 part household bleach to 9 parts water, and not donating blood or semen. ^[2]

The modern standard is oral, usually 8 or 12 weeks, pangenotypic direct-acting antivirals with cure rates above 95%. ^{[1] [2]} DAA therapy improves liver outcomes (reduced all-cause mortality, cirrhosis, decompensation and hepatocellular carcinoma) and the extrahepatic manifestations, and should be offered to all adults with acute or chronic HCV infection, except those with a life expectancy too short to be altered by treatment. ^[2] People who inject drugs, people with ongoing alcohol use and people with psychiatric illness are not excluded, and achieve cure rates comparable with other groups when adherence is maintained. ^[2]

AASLD-IDSA provides a simplified treatment algorithm for treatment-naive adults, usable by non-specialists with specialist support available. It applies when there is evidence of either no cirrhosis or compensated cirrhosis. It excludes people with HIV or hepatitis B coinfection, prior liver transplantation, hepatocellular carcinoma, end-stage renal disease (eGFR below 30 mL per min), and current pregnancy. ^[2]

Pre-treatment checks in the simplified pathway: assess cirrhosis, review medications and drug-drug interactions, confirm chronic infection (quantitative HCV RNA), test for HIV antigen/antibody and hepatitis B surface antigen, check complete blood count, international normalised ratio, liver function and estimated glomerular filtration rate, test for pregnancy where relevant, and evaluate for decompensation (ascites, encephalopathy, Child-Turcotte-Pugh class) with liver ultrasound within the prior 6 months in people with cirrhosis. ^[2]

During treatment, on-treatment blood monitoring is usually unnecessary for people without cirrhosis who feel well, other than glucose and international normalised ratio monitoring in people taking diabetes medicines or warfarin. ^[2]

Treatment response. HCV RNA and liver transaminases are tested 12 weeks or more after the last dose. Undetectable HCV RNA at that point is a sustained virologic response (SVR), defined as cure. ^[2] Real-world and trial data support above 95% cure rates with these regimens. ^{[1] [2]}

Follow-up then differs by liver status:

• No cirrhosis and SVR: no liver-specific follow-up is needed. People with ongoing risk behaviour should receive harm-reduction counselling and annual HCV RNA testing (or testing when transaminases rise). ^[2]
• Compensated cirrhosis and SVR: ultrasound surveillance for hepatocellular carcinoma every 6 months, with or without alpha-fetoprotein, regardless of cure, plus endoscopic surveillance for oesophageal varices according to AASLD guidance. Continue alcohol abstinence and harm-reduction counselling. ^[2]

Recurrent HCV RNA after SVR is either reinfection (treat again as for a first infection) or late relapse (refer to a specialist). ^[2]

People with decompensated cirrhosis (Child-Turcotte-Pugh class B or C), or any history of decompensation, do not fit the simplified algorithm and need specialist management. ^[2] They require assessment for liver transplantation as well as antiviral therapy, because successful treatment can improve liver function and alter candidacy and anticoagulation. For people with hepatocellular carcinoma the approach is similarly individualised, and antiviral therapy is still recommended where it can be delivered safely. ^[2]

HIV and HCV coinfection is common given shared transmission routes, and it predicts faster fibrosis progression. ^[3] The simplified algorithm above is not recommended for people with HIV; they should be treated with DAAs, but under a provider who checks drug-drug interactions with antiretroviral therapy and stages fibrosis. ^[2] Anyone with chronic hepatitis C who is HIV-negative should be offered hepatitis B vaccination and counselling to avoid HIV acquisition, and HIV testing is part of the baseline work-up. ^[2]

Chronic hepatitis C is itself a risk factor for chronic kidney disease, and the most frequent renal association is membranoproliferative glomerulonephritis, usually driven by mixed cryoglobulinaemic vasculitis. ^[6] DAAs are effective in people with chronic kidney disease, including those on dialysis, with sustained virologic response rates of 93% to 100% and acceptable safety. ^[6] No dose adjustment of the direct-acting antivirals is needed in renal impairment, although a ribavirin dose reduction may be required where ribavirin is used in older or alternative regimens. ^[6] Sofosbuvir is now approved for use with estimated glomerular filtration rate at or below 30 mL per min or on dialysis, glecaprevir/pibrentasvir has been studied extensively in dialysis-dependent people, and elbasvir/grazoprevir is an option in genotype 1 or 4 infection with severe renal impairment. ^[6]

Practical interaction reminders from this population include colchicine-induced rhabdomyolysis reported with glecaprevir/pibrentasvir, and atorvastatin-related muscle toxicity, especially with pre-existing renal dysfunction; those starting DAA therapy while on colchicine or a statin should have the drug-dose reviewed. ^[6]

Direct-acting antivirals are not approved for use in pregnancy; safety data are preliminary. ^[3] Care is therefore arranged around the mother rather than the pregnancy. Mothers identified during pregnancy should be linked to treatment after delivery, which also reduces transmission risk in future pregnancies. ^[3] Pregnancy is still a useful time to find infection: many women only have access to care during pregnancy and the postpartum period, and testing at the same time as other prenatal infection screens is convenient. ^[3] People with hepatitis C in pregnancy should be advised about delivery practices (avoiding prolonged rupture of membranes, internal fetal monitoring and episiotomy unless necessary) and breastfeeding is not contraindicated unless nipples are cracked or bleeding. ^[3] Caesarean delivery is not indicated for hepatitis C. ^[3]

For the infant, HCV RNA testing is possible from 2 months of age, and anti-HCV antibody testing at or after 18 months. ^[3] Only about 20% of infants with perinatally acquired hepatitis C clear the infection; about half have chronic asymptomatic infection and 30% chronic active infection. ^[3] Mother-to-child transmission occurs in about 5% to 6% of births and roughly doubles with maternal HIV coinfection. ^{[2] [3]} Children with vertical infection should be evaluated for spontaneous clearance, since about a quarter to half of infected infants clear the virus by 4 years. ^[2]

In children, direct-acting antivirals are now licensed for age 3 years and above. ^[3] When to treat in younger or asymptomatic children should be individualised with specialist input.

Most treatment failures today are relapses or reinfections in an era of high efficacy. A person in whom initial DAA therapy fails should be evaluated by a clinician experienced in HCV treatment failure before retreatment, because regimen and duration depend on the original drug, genotype, cirrhosis status and resistance-associated substitutions. ^[2] The principle is that retreatment often succeeds with a different combination (for example a salvage regimen of sofosbuvir plus glecaprevir/pibrentasvir with ribavirin for multiple DAA failures). ^[2] If retreatment must be delayed, liver disease progression should be assessed every 6 to 12 months. ^[2]

Direct-acting antivirals are metabolised in the liver and interact with other drugs. Any regimen requires a formal drug-drug interaction check, especially for people on antiretrovirals, immunosuppressants, antiarrhythmics, direct oral anticoagulants, statins, anticonvulsants and rifamycins. ^{[2] [6]} Two interactions recur in the guidance: treatment may lower blood glucose in people with diabetes (warn patients about possible hypoglycaemia) and may reduce the effect of warfarin (monitor international normalised ratio). ^[2] Genotype 3 infection with baseline (pretreatment) NS5A resistance testing is needed before sofosbuvir/velpatasvir in compensated cirrhosis. ^[2]

• Cirrhosis: develops in an estimated 15% to 30% (WHO) or 5% to 25% (CDC) of people with chronic infection within 20 years, more often with alcohol use, metabolic disease and coinfections. ^{[1] [3]}
• Hepatocellular carcinoma: 1% to 4% per year once cirrhosis is present; risk falls but does not disappear after sustained virologic response. ^{[2] [3]}
• Hepatic decompensation: ascites, variceal bleeding, encephalopathy in advanced cirrhosis. ^[2]
• Extrahepatic disease: mixed cryoglobulinaemia with palpable purpura, arthralgia, neuropathy and glomerulonephritis; B-cell lymphoma; porphyria cutanea tarda; lichen planus; thyroid disease; type 2 diabetes. ^[5]
• Post-treatment reinfection: possible in people with ongoing injecting or other risk behaviours; treat again as first infection. ^[2]

Cure is the norm for people who receive treatment. Direct-acting antiviral therapy achieves sustained virologic response in more than 95% of people, including most people with cirrhosis. ^{[1] [2]} After cure, all-cause mortality, cirrhosis and hepatocellular carcinoma all fall, although not to the level of never-infected people when cirrhosis was already present. ^[2] People with cirrhosis still need cancer surveillance and variceal assessment after cure. ^[2] People who are untreated remain at risk for cirrhosis, liver cancer and premature death; in the United States chronic hepatitis C is a major cause of liver-related death and transplantation need. ^[3]

People with chronic hepatitis C also face higher all-cause and non-liver mortality linked to extrahepatic manifestations, which is another reason to treat early. ^[5]

Screening is what finds the disease, because most infection is silent. The approaches differ by country, but the consensus is broad:

• Universal adult screening. In the United States, the CDC recommends hepatitis C screening at least once in a lifetime for all adults aged 18 years and over, except in settings where HCV RNA prevalence is documented below 0.1%. ^[3] The US Preventive Services Task Force recommends one-time screening for adults aged 18 to 79 years, with anti-HCV antibody followed by confirmatory RNA testing, and periodic screening for people with continued risk. ^[4] The AASLD-IDSA guidance recommends one-time, routine, opt-out screening for all individuals aged 18 years and over, without an upper age limit. ^[2]
• Every pregnancy. CDC recommends hepatitis C screening during each pregnancy, with the same prevalence threshold. ^[3] The US Preventive Services Task Force includes pregnant persons in the adult recommendation. ^[4]
• People at ongoing risk. People who inject drugs should be screened periodically (at least annually), as should men with HIV who have unprotected sex with men. ^{[2] [3]} Anyone with risk factors should be tested whatever their age, with periodic testing while risk persists. ^[3]
• Anyone who asks. Anyone who requests testing should receive it, regardless of disclosure of risk. ^[3]
• Diagnostic algorithm (above): anti-HCV antibody with reflex HCV RNA. Blood banks screen all donations. ^[3]
• WHO recommends offering general population testing in adolescents and adults in settings with intermediate or high (above 2%) anti-HCV seroprevalence, and targeted testing for risk groups everywhere (people who inject drugs, prisoners, men who have sex with men, sex workers, people with HIV or tuberculosis, migrants from endemic areas, health workers, blood donors, people with liver disease). ^[1]

There is no vaccine against hepatitis C, and no effective pre-exposure or post-exposure prophylaxis (immune globulin is not recommended). ^{[1] [3] [7]} After an occupational exposure (for example a needlestick from an HCV-positive source) the recommended approach is monitoring and early treatment if infection occurs: HCV RNA at 3 to 6 weeks, and anti-HCV at 4 to 6 months, with treatment of any new infection using direct-acting antivirals. ^[7] The risk of HCV transmission after a percutaneous exposure is low (about 0.2% in recent CDC data, about 1.8% in older literature) and mucocutaneous exposure effectively zero, so treating every exposed person would not be cost-effective. ^[7] The same monitoring approach applies after non-occupational exposure.

Low- and middle-income countries carry most of the global burden, and elimination there depends on simplifying delivery rather than on specialist clinics.

• Generic drugs. Pan-genotypic direct-acting antivirals are expensive in many high- and upper-middle-income countries, but generic versions have driven the price of a standard curative course below US$ 50 in many low- and middle-income countries, most commonly sofosbuvir with daclatasvir. ^[1]
• Task-shifting and decentralisation. WHO recommends that testing, care and treatment can be delivered by trained non-specialist doctors and nurses in primary care, harm reduction services and prisons, with minimal on-treatment monitoring. ^[1]
• Decentralised testing. Point-of-care HCV RNA tests (for example dried blood spot or cartridge-based RNA) allow confirmation of infection outside referral hospitals, which is critical where people live far from a laboratory. ^[1]
• Egypt and similar programmes. Egypt's mass screening and treatment campaign, using cheap generic direct-acting antivirals, has cut prevalence dramatically. It remains the model for large-scale viral elimination using generic drugs. ^[1]
• Harm reduction. Needle and syringe programmes, opioid agonist therapy (methadone or buprenorphine), safe-injection counselling and safe disposal reduce transmission among people who inject drugs and in prisons. ^[1]
• Infection control and blood safety. Reuse of therapeutic syringes and unscreened transfusion are still major drivers of new infection in some regions. Safe injection practice and universal blood screening come first. ^[1]

• Hepatitis C is a curable blood-borne liver infection. Around 47 million people live with chronic disease worldwide. ^[1]
• HCV spreads by contact with infected blood: injecting equipment sharing, unsafe healthcare injections, and unscreened transfusions before 1992 are the main routes. ^{[1] [3]}
• About 30% of acutely infected people clear the virus; 70% develop chronic infection; estimates of cirrhosis risk are 15% to 30% within 20 years (WHO) or 5% to 25% over 10 to 20 years (CDC); cirrhosis carries roughly 1% to 4% annual risk of hepatocellular carcinoma. ^{[1] [3]}
• The disease is usually silent; screening (antibody, then RNA) is the only way to find it. ^{[2] [3]}
• Modern direct-acting antivirals are taken by mouth for 8 or 12 weeks and cure more than 95% of infections, with the same strategy for treated and untreated people. ^{[1] [2]}
• There is no vaccine and no post-exposure prophylaxis; prevention rests on blood and injection safety plus harm reduction. ^{[1] [3]}
• A sustained virologic response (undetectable HCV RNA 12 weeks after treatment) is a cure, but people with cirrhosis still need 6-monthly liver ultrasound for cancer. ^[2]
• Hepatitis B, HIV, renal function, pregnancy and alcohol status should be checked before treatment; direct-acting antivirals are not approved in pregnancy. ^{[3] [6]}
• Many effective regimens are now generic and cheap, allowing nurse- and physician-supervised treatment in primary care. ^[1]

Plain text only: Hepatitis B; Cirrhosis and portal hypertension; Hepatocellular carcinoma; HIV infection; Chronic kidney disease; Cryoglobulinaemia; Liver transplantation; Alcohol use disorder; Vaccination. Drug topics: direct-acting antivirals (see hepatology and infectious disease formularies).