Hepatitis C

Table of Contents

1. Overview: The Silent Liver Epidemic
2. Transmission and Risk Factors
3. How HCV Damages the Liver: Pathophysiology and Genotypes
4. Acute vs. Chronic Infection
5. Symptoms and Extrahepatic Manifestations
6. Diagnosis and Monitoring
7. Treatment with Direct-Acting Antivirals
8. Outcomes After SVR (Cure)
9. Prevention and Public Health
10. Research Papers
11. Connections
12. Featured Videos

Overview: The Silent Liver Epidemic

Hepatitis C is a chronic liver infection caused by the hepatitis C virus (HCV) — a small, single-stranded RNA virus in the Flaviviridae family. It is one of the most important infectious liver diseases in the world, affecting an estimated 58 million people with chronic infection globally and approximately 2.4 million people in the United States — though millions more remain undiagnosed because the disease causes no symptoms for decades.

What makes hepatitis C so dangerous and so underestimated is that it is almost completely silent. Most people who contract HCV feel perfectly normal for 20 to 30 years while the virus steadily damages their liver. By the time symptoms appear — jaundice, severe fatigue, swollen abdomen — the liver may already be in end-stage failure. Historically, hepatitis C was the leading cause of liver transplantation in the United States. It remains a major driver of hepatocellular carcinoma (liver cancer) worldwide.

The critical turning point came in 2014, when an entirely new class of medications called direct-acting antivirals (DAAs) transformed hepatitis C from a difficult-to-treat, sometimes fatal disease into a curable infection. Today, short courses of DAA pills — typically 8 to 12 weeks — cure hepatitis C in 95–99% of patients, with minimal side effects. The challenge now is not treatment, but finding the millions of people who don't know they are infected.

HCV comes in six major genotypes (genetic variants), numbered 1 through 6. Genotype 1 accounts for the majority of infections in the United States and was historically the hardest to treat. Modern pangenotypic DAAs work against all genotypes, making genotype testing less critical for treatment decisions but still performed for regimen selection. The 75–85% of people exposed to HCV who do not spontaneously clear the virus go on to develop chronic infection — defined as detectable virus in the blood for more than 6 months.

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Transmission and Risk Factors

HCV spreads through direct blood-to-blood contact. It is not transmitted through casual contact — you cannot get it from hugging someone, sharing food or water, kissing, coughing, sneezing, or using the same bathroom. Understanding the actual routes helps identify who needs testing and how to prevent new infections.

High-Risk Routes

• Injection drug use — this is by far the most common route of new HCV infections in the United States today, accounting for the large majority of new cases. Sharing needles, syringes, cookers, cotton filters, or any equipment used to prepare or inject drugs transmits the virus with high efficiency. A single shared needle carries meaningful risk.
• Blood transfusion or organ transplant before 1992 — before routine blood supply screening began in 1992, transfused blood frequently contained HCV. Anyone who received a transfusion or transplant before that year should be tested. This is why Americans born between 1945 and 1965 (baby boomers) have a hepatitis C prevalence roughly 5 times higher than other age groups — many were exposed through contaminated blood before testing existed.
• Needlestick injuries in healthcare settings — occupational exposure remains a real risk. The average seroconversion rate after a needlestick from an HCV-positive patient is approximately 1.8% — lower than hepatitis B but significantly higher than HIV.

Lower-Risk Routes

• Tattooing and body piercing — when performed with non-sterile equipment, there is a documented but relatively lower risk. Licensed studios with proper sterilization protocols carry minimal risk.
• Sexual transmission — HCV can be transmitted sexually, but the risk is low in long-term monogamous heterosexual relationships. Risk increases significantly with HIV co-infection and among men who have sex with men (MSM) with multiple partners, particularly with practices that involve mucosal trauma or blood exposure.
• Mother to child (perinatal) — transmission from an HCV-positive mother to her baby during birth occurs in approximately 4–8% of pregnancies. The rate is higher if the mother is also HIV-positive.
• Sharing personal items — items that might have blood on them, such as razors or toothbrushes, can theoretically transmit HCV if shared, though this is uncommon in practice.
• Intranasal drug use — sharing straws or tubes for snorting cocaine or other drugs can transmit HCV if nasal mucosa is damaged and instruments are shared.

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How HCV Damages the Liver: Pathophysiology and Genotypes

Understanding how HCV causes liver damage helps explain why the disease is silent for so long and why treatment matters even when you feel fine.

How the Virus Works

HCV targets hepatocytes — the primary working cells of the liver — by entering them through the CD81 receptor on the cell surface. Once inside, the virus uses the cell's own machinery to replicate, producing billions of viral copies daily. HCV is exceptionally skilled at evading the immune system: its surface protein (the hypervariable region 1) mutates rapidly, staying ahead of antibodies; and one of its key enzymes — the NS3/4A protease — actively dismantles the cell's innate immune alarm system by cleaving two critical signaling proteins (MAVS and TRIF) that normally would trigger an antiviral response. The result is that the immune system can neither eliminate the virus nor ignore it — it mounts a chronic, low-grade inflammatory response that persists for decades.

This chronic inflammation is what damages the liver. Over years, inflammatory signals activate liver cells called hepatic stellate cells, which respond by laying down scar tissue — a process driven by transforming growth factor-beta (TGF-β). Scar tissue replaces functional liver tissue in a process called fibrosis. When fibrosis becomes widespread and the liver's architecture is restructured into nodules surrounded by scar bands, it becomes cirrhosis — an irreversible (though partially reversible after cure) late stage associated with liver failure, portal hypertension, and liver cancer.

The Six Genotypes

HCV exists as six major genotypes (GT1–GT6), each with distinct geographic distributions and subtleties in treatment response:

• Genotype 1 (GT1) — the most common worldwide and in the United States, accounting for approximately 70% of US infections. GT1a and GT1b are the two main subtypes; GT1a has more naturally occurring resistance variants in the NS5A region that historically affected treatment with some regimens. All GT1 infections respond excellently to modern pangenotypic DAAs.
• Genotype 2 (GT2) — common in the US and Europe; has consistently excellent treatment outcomes.
• Genotype 3 (GT3) — prevalent in South Asia and increasingly in Europe and the US through injection drug use; associated with higher rates of liver fat deposition (steatosis) independently of HCV; slightly more challenging with some DAA combinations, particularly in patients with cirrhosis.
• Genotypes 4–6 — GT4 is most common in the Middle East and Africa; GT5 in South Africa; GT6 in Southeast Asia. All are less common in the US but respond to pangenotypic DAAs.

While genotyping remains standard practice before treatment, modern pangenotypic regimens like glecaprevir/pibrentasvir and sofosbuvir/velpatasvir work across all six genotypes, making the genotype result primarily useful for fine-tuning regimen duration rather than selecting among fundamentally different drug classes.

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Acute vs. Chronic Infection

HCV infection passes through two phases. Understanding the distinction matters for testing timing, prognosis, and the small window of opportunity for spontaneous recovery.

Acute Hepatitis C (0–6 Months)

The acute phase encompasses the first six months after exposure. The vast majority of people — roughly 70–80% — have no symptoms at all during this phase. The remaining 20–30% may experience fatigue, nausea, abdominal discomfort, or mild jaundice, typically appearing 2–12 weeks after exposure. Acute HCV is rarely diagnosed because symptoms are absent or nonspecific and most people don't know they were exposed.

Approximately 15–25% of people who contract HCV do clear the virus spontaneously during the acute phase, without treatment. Factors that favor spontaneous clearance include female sex, symptomatic presentation during acute infection (paradoxically, feeling sick means a stronger immune response), younger age at infection, and a favorable genetic variant in the IL28B gene (CC genotype), which encodes interferon-lambda. If the virus is still detectable in the blood at six months, spontaneous clearance becomes extremely unlikely.

Chronic Hepatitis C (Beyond 6 Months)

The 75–85% of infected people who don't clear the virus develop chronic hepatitis C. Chronic infection is defined by the persistence of HCV RNA in the blood for more than six months. This phase is where the real damage occurs — but it happens slowly and silently. Most people feel entirely well for 20 to 30 years while fibrosis gradually accumulates. On average, progression from infection to cirrhosis takes 20–30 years, but there is enormous individual variation.

Cofactors That Accelerate Fibrosis

Several factors cause fibrosis to progress much faster in some people than others:

• Alcohol use — the single most important modifiable accelerant. Even moderate alcohol consumption (as little as 30g/day in men, less in women) doubles or triples the rate of fibrosis progression. Stopping alcohol is the most impactful lifestyle change a person with chronic HCV can make while awaiting treatment.
• HIV co-infection — dramatically accelerates fibrosis, with progression to cirrhosis occurring 3–5 times faster than in HIV-negative patients. HIV-HCV co-infected individuals should be prioritized for early treatment.
• Hepatitis B co-infection — dual hepatitis B and C infection worsens liver outcomes and increases liver cancer risk.
• Metabolic syndrome and fatty liver disease (MASLD) — liver fat and insulin resistance both accelerate HCV-related fibrosis. The convergence of the obesity epidemic and existing HCV infections has created a significant burden of combined disease.
• Older age at infection and male sex — fibrosis progresses more rapidly in people infected after age 40 and in men compared to women.
• Immunosuppression — organ transplant recipients and others on immunosuppressive medications experience accelerated HCV progression.

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Symptoms and Extrahepatic Manifestations

Hepatitis C is sometimes called the "silent epidemic" precisely because most people have no liver symptoms until the disease is very advanced. But the virus does not confine its effects to the liver — a remarkable range of conditions throughout the body are directly caused or triggered by chronic HCV infection.

Liver Symptoms

During the decades of chronic infection, most people feel well. When liver symptoms do occur, they typically signal significant fibrosis or decompensated cirrhosis:

• Fatigue — the most common complaint reported by people with chronic HCV, and it does not always correlate with the degree of liver damage. Many patients describe profound, life-limiting fatigue even without advanced fibrosis.
• Right upper quadrant discomfort — a dull ache or heaviness under the right ribs can occur as the liver enlarges or becomes inflamed.
• Jaundice — yellowing of the skin and eyes, indicating significant liver dysfunction; may occur during acute infection or in decompensated cirrhosis.
• Signs of cirrhosis — ascites (fluid in the abdomen), leg edema, spontaneous bruising, confusion (hepatic encephalopathy), and vomiting blood from esophageal varices represent late-stage disease.

Extrahepatic Manifestations

What many people don't realize is that chronic HCV infection affects many organ systems beyond the liver — an estimated 40–75% of patients have at least one extrahepatic manifestation. These are not incidental — they are directly caused by the virus or by the immune response to it:

• Mixed cryoglobulinemia — HCV is the most common cause of mixed (type II) cryoglobulinemia. Cryoglobulins are abnormal immune complexes that form in response to chronic HCV stimulation of B cells and precipitate in cold temperatures, depositing in small blood vessels and causing vasculitis. The clinical triad includes palpable purpura on the legs (the skin finding), peripheral neuropathy (painful or numb hands/feet), and arthralgia (joint pain). Severe cases cause kidney damage (membranoproliferative glomerulonephritis). Treating and curing HCV with DAAs typically resolves cryoglobulinemia.
• B-cell lymphoma — HCV chronically stimulates B cells through the CD81 receptor, increasing the risk of B-cell non-Hodgkin lymphoma (NHL) by 2–3 fold. SVR after DAA treatment reduces this risk.
• Thyroid disease — autoimmune thyroiditis (including Hashimoto's thyroiditis) is significantly more common in people with chronic HCV, particularly women. Thyroid function testing is reasonable in HCV-positive patients with fatigue or other suggestive symptoms.
• Type 2 diabetes — HCV impairs hepatic insulin signaling, increasing the risk of type 2 diabetes roughly 3-fold compared to the general population. The association is especially strong with genotype 3. SVR improves insulin sensitivity.
• Oral lichen planus — chronic white, lacy patches or painful erosions on the inner cheeks and tongue; HCV is one of the most recognized triggers.
• Sicca syndrome — dry eyes and dry mouth resembling Sjögren's syndrome occur in a subset of HCV patients and are thought to be immune-mediated.
• Porphyria cutanea tarda (PCT) — HCV and iron excess together trigger PCT, causing blistering, fragile skin on sun-exposed areas, particularly the hands. HCV is the most common infectious trigger of PCT.

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Diagnosis and Monitoring

Because hepatitis C causes no symptoms for decades, the path to diagnosis almost always runs through screening — either routine universal testing or targeted testing of high-risk groups. A simple blood test sequence confirms the diagnosis and characterizes the infection.

Who Should Be Screened

The US Preventive Services Task Force (USPSTF) issued an A recommendation in 2020 for universal one-time HCV screening in all adults aged 18–79, regardless of risk factors. Beyond this universal recommendation, certain groups should be screened more frequently:

• People who currently inject drugs or have done so in the past — annual screening recommended
• People with HIV — annual HCV screening recommended
• Adults born between 1945 and 1965 (baby boomers) — one-time screening if not already performed
• Recipients of blood transfusions or organ transplants before 1992
• People who have been incarcerated (higher HCV prevalence in correctional facilities)
• Hemodialysis patients
• Children born to HCV-positive mothers

The Testing Sequence

HCV testing follows a two-step approach:

1. Anti-HCV antibody test (step 1) — this blood test detects antibodies your immune system made against HCV. It becomes positive 8–11 weeks after exposure. A reactive (positive) result means you have been exposed to HCV at some point — but it does not distinguish between a past infection that cleared and a current active infection. The antibody stays positive for life even after cure. In immunocompromised patients (such as those on dialysis or with HIV), antibody tests can occasionally give false-negative results.
2. HCV RNA by PCR (step 2, if antibody is reactive) — this test detects the actual virus in the blood. It becomes positive within 1–2 weeks of exposure. A detectable HCV RNA confirms active infection. Quantitative testing measures the viral load (number of viral copies per milliliter), which helps monitor treatment response. Genotyping is then performed on the same sample.

Assessing Fibrosis (Without a Biopsy)

Determining how much liver damage has occurred is essential for treatment decisions and surveillance planning. Liver biopsy — once the gold standard — is now rarely needed because non-invasive tests are accurate and widely available:

• FIB-4 index — calculated as: (Age × AST) ÷ (Platelets × √ALT). A score below 1.45 reliably rules out significant fibrosis; a score above 3.25 suggests advanced fibrosis or cirrhosis. This simple calculation from routine blood tests is the recommended first-line fibrosis assessment.
• APRI score (AST-to-Platelet Ratio Index) — another serum-based score, less precise than FIB-4 but widely used.
• FibroScan / transient elastography (VCTE) — a painless ultrasound-based device that measures liver stiffness (stiff liver = more scar tissue). Provides a direct measurement of fibrosis stage with excellent accuracy, especially for confirming cirrhosis.

Liver Cancer Surveillance

Patients with established cirrhosis — even after achieving a cure — require ongoing surveillance for hepatocellular carcinoma (HCC) with abdominal ultrasound every 6 months. Cirrhosis does not fully reverse after SVR, and the HCC risk in cirrhotic patients, while substantially reduced, remains elevated for life (approximately 1–1.5% per year). Surveillance allows detection of HCC at an early, treatable stage.

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Treatment with Direct-Acting Antivirals

The treatment of hepatitis C has undergone a complete revolution since 2014. Before direct-acting antivirals, treatment required injecting interferon three times per week for up to 48 weeks, caused severe flu-like side effects, and cured only 40–50% of patients with the most common genotype. Today's DAAs are short courses of oral pills — taken once or twice daily for 8 to 12 weeks — that achieve cure in 95–99% of patients with minimal side effects.

What "Cure" Means: Sustained Virologic Response (SVR)

Treatment success is defined as sustained virologic response (SVR) — undetectable HCV RNA in the blood 12 weeks after completing treatment. SVR12 is considered a functional cure: the virus does not return in the vast majority of patients, liver inflammation resolves, and the long-term consequences of ongoing infection are prevented. SVR is not the same as immunity — reinfection from new exposure is possible, especially in people who inject drugs, and re-treatment is effective.

Current Standard DAA Regimens

• Glecaprevir/pibrentasvir (Mavyret) — a pangenotypic combination (works against GT1–6) combining an NS3/4A protease inhibitor with an NS5A inhibitor. For treatment-naive patients without cirrhosis: 8 weeks. For patients with compensated cirrhosis: 12 weeks. One of the shortest available treatment courses. Well-tolerated; most common side effects are headache, fatigue, and nausea. Contraindicated in decompensated (Child-Pugh B/C) cirrhosis.
• Sofosbuvir/velpatasvir (Epclusa) — pangenotypic combination (GT1–6) of an NS5B polymerase inhibitor and an NS5A inhibitor. Standard course: 12 weeks for most patients. For GT3 with cirrhosis, adding ribavirin for 12 weeks or extending to 24 weeks (without ribavirin) improves outcomes. First choice in many international guidelines.
• Sofosbuvir/ledipasvir (Harvoni) — approved for GT1, 4, 5, and 6. Treatment-naive GT1 patients without cirrhosis with low viral load can be treated in 8 weeks; standard is 12 weeks. Has an extensive real-world track record from the early DAA era.
• Elbasvir/grazoprevir (Zepatier) — approved for GT1 and GT4. Requires NS5A resistance testing before use in GT1a patients (about 10–15% have resistance variants that reduce efficacy). Uniquely useful for patients with severe kidney disease (GFR <30) — unlike sofosbuvir-containing regimens, it is safe and does not require dose adjustment in advanced CKD.

Treatment in Special Populations

• Chronic kidney disease / dialysis — avoid sofosbuvir-containing regimens when GFR is below 30 mL/min (sofosbuvir accumulates and may worsen kidney function). Use elbasvir/grazoprevir or glecaprevir/pibrentasvir instead, both of which are renally safe.
• Decompensated cirrhosis (Child-Pugh B or C) — glecaprevir/pibrentasvir is contraindicated. Use sofosbuvir/velpatasvir ± ribavirin. These patients require specialist management and may need liver transplant evaluation in parallel with treatment.
• Post-liver transplant — DAAs are safe and highly effective after transplant. Drug interactions with immunosuppressants (especially tacrolimus and cyclosporine) require careful monitoring and possible dose adjustment, but this is manageable with specialist guidance.
• Pregnancy — DAAs are generally deferred until after delivery because safety data in pregnancy are limited. Ribavirin is absolutely contraindicated in pregnancy (causes birth defects) and for 6 months after treatment in both partners. Screening and linkage to care during pregnancy allows prompt treatment after delivery.
• HIV co-infection — HCV treatment is as effective in HIV-positive patients as in HIV-negative patients when antiretroviral therapy is well-controlled. Check for drug-drug interactions between DAAs and antiretroviral medications; many combinations are safe but some (particularly certain HIV protease inhibitors and efavirenz) require regimen adjustment.

What Treatment Doesn't Do

DAAs cure HCV infection but do not reverse established cirrhosis (though fibrosis can regress meaningfully after SVR), do not eliminate the need for ongoing HCC surveillance in cirrhotic patients, do not protect against reinfection from new HCV exposure, and do not treat any complications of advanced cirrhosis (such as varices or ascites), which require separate management.

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Outcomes After SVR (Cure)

Achieving SVR — a cure of HCV infection — has profound and lasting benefits that extend far beyond simply clearing the virus from the blood. Long-term studies consistently show that SVR translates into real, measurable improvements in liver health, cancer risk, and survival.

What Happens to the Liver After Cure

• Inflammation resolves — liver enzyme levels (ALT, AST) normalize within weeks of completing treatment in most patients, reflecting the end of active viral inflammation.
• Fibrosis regression — fibrosis actively reverses after SVR. Studies using FibroScan and liver biopsy confirm measurable reductions in liver stiffness in the majority of patients over 1–5 years after cure, including patients with F3 and even F4 (cirrhotic) fibrosis. The liver has genuine capacity for self-repair when the viral insult is removed. The degree of regression is greater in patients with less advanced fibrosis at the time of treatment.
• Liver cancer risk dramatically reduced — SVR is associated with a 70% or greater reduction in the risk of hepatocellular carcinoma compared to patients who do not achieve SVR. This is one of the strongest cancer-prevention effects of any antiviral treatment known in medicine. However, in patients who already have cirrhosis, the HCC risk remains elevated even after cure (at approximately 1–1.5%/year) and requires lifelong surveillance.

Systemic Benefits Beyond the Liver

• Cryoglobulinemia remission — mixed cryoglobulinemia, including its vasculitic complications (purpura, neuropathy, kidney disease), typically remits or significantly improves after HCV cure. This is one of the most dramatic examples of treating an extrahepatic manifestation by curing its root cause.
• Improved insulin sensitivity — type 2 diabetes risk decreases after SVR, and some patients with existing diabetes see improved glycemic control.
• Reduced lymphoma risk — the elevated risk of B-cell NHL associated with chronic HCV infection falls after cure.
• Fatigue improvement — many patients report significant improvement in fatigue and quality of life after achieving SVR, even when laboratory values were only mildly abnormal before treatment.

Survival Benefit

Multiple large studies — both in VA populations (Backus 2011) and in European cohorts (van der Meer 2012) — have shown that SVR is associated with a 50% or greater reduction in all-cause mortality compared to patients who do not achieve SVR. This includes reductions in liver-related deaths, cardiovascular deaths, and deaths from extrahepatic manifestations. The survival benefit is largest in patients with advanced fibrosis, who have the most to gain from treatment.

Reinfection

SVR is a cure of the existing infection, not immunity. If a person is re-exposed to HCV — through continued injection drug use or other routes — they can acquire a new infection. Reinfection rates are significant in people who inject drugs. Re-treatment with DAAs is equally effective for reinfection as for primary infection, and reinfection is not a reason to withhold initial treatment from people who use drugs.

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Prevention and Public Health

Unlike hepatitis A and hepatitis B, there is no vaccine for hepatitis C. The RNA virus mutates so rapidly that developing an effective vaccine has proven extraordinarily difficult, and research continues. Prevention therefore depends entirely on interrupting transmission, identifying infected people through screening, and linking them to curative treatment.

Harm Reduction

Because injection drug use drives the overwhelming majority of new HCV infections in the US, harm reduction programs are the most powerful tools for prevention:

• Needle/syringe service programs (SSPs) — programs that provide clean injection equipment to people who use drugs reduce HCV transmission without increasing drug use. They also serve as access points for testing, treatment referral, naloxone distribution, and social services.
• Opioid agonist therapy (OAT) — medications such as methadone and buprenorphine treat opioid use disorder and reduce injection drug use and associated HCV transmission.
• Education on safer use — using single-use, sterile needles and syringes every time; never sharing any injection equipment (including cookers, cotton, water, and ties); and cleaning injection sites reduces transmission risk substantially.

Healthcare Worker Protection

Standard precautions — gloves, eye protection, safe needle handling, and proper sharps disposal — remain the foundation of occupational HCV prevention. Unlike HIV, there is no post-exposure prophylaxis (PEP) regimen proven to prevent HCV after a needlestick. The recommended post-exposure protocol is baseline HCV RNA testing at the time of exposure, followed by repeat HCV RNA at 2–4 weeks and 12 weeks, and anti-HCV antibody at 6 months. If HCV RNA becomes detectable, prompt referral for DAA treatment achieves cure before chronic infection establishes.

Universal Screening and Treatment as Prevention

The 2020 USPSTF A recommendation for universal adult screening represents a major public health advance. Identifying and treating people with HCV not only benefits the individual but also removes them from the pool of people who can transmit the virus — treatment is prevention. Universal screening substantially increases the proportion of infected people who are diagnosed, which is the first step to cure.

Global Elimination Goal

The World Health Organization has set a goal of eliminating hepatitis C as a public health threat by 2030 — defined as an 80% reduction in new HCV infections and a 65% reduction in HCV-related mortality compared to 2015 levels. Some high-income countries (Iceland, Australia, Egypt) have made remarkable progress toward these goals. The central remaining challenge is access: DAA regimens cost thousands of dollars per course in the US (though generic versions are available in some countries for under $100), and in many low- and middle-income countries, most people with HCV still cannot access treatment. Closing this access gap is the defining public health challenge of HCV elimination.

Sexual Prevention

For people in long-term monogamous heterosexual relationships where one partner has HCV, the risk of sexual transmission is low enough that barrier methods are not universally required, though they are sensible. For people with multiple partners, MSM with HIV co-infection, or people whose sexual practices carry higher blood exposure risk, consistent condom use is recommended. People with HCV who are in serodiscordant relationships (one partner HCV-positive, one negative) should discuss the specific risk level and protective measures with their healthcare provider.

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Research Papers

1. Polaris Observatory HCV Collaborators. Global prevalence and genotype distribution of hepatitis C virus infection in 2015. Lancet Gastroenterol Hepatol. 2017;2:161-176. PMID 28404132. DOI: 10.1016/S2468-1253(16)30181-9
2. Zeuzem S et al. Glecaprevir-Pibrentasvir for 8 or 12 Weeks in HCV Genotype 1 or 3 Infection. N Engl J Med. 2018;378:354-369. PMID 29342396. DOI: 10.1056/NEJMoa1702417
3. Feld JJ et al. Sofosbuvir and Velpatasvir for HCV Genotype 1, 2, 4, 5, and 6 Infection. N Engl J Med. 2015;373:2599-2607. PMID 26571066. DOI: 10.1056/NEJMoa1512610
4. Afdhal N et al. Ledipasvir and Sofosbuvir for Untreated HCV Genotype 1 Infection. N Engl J Med. 2014;370:1889-1898. PMID 24725239. DOI: 10.1056/NEJMoa1402454
5. van der Meer AJ et al. Association Between Sustained Virological Response and All-Cause Mortality Among Patients With Chronic Hepatitis C and Advanced Hepatic Fibrosis. JAMA. 2012;308:2584-2593. PMID 23268517. DOI: 10.1001/jama.2012.144071
6. Cacoub P et al. Extrahepatic manifestations associated with hepatitis C virus infection. Medicine (Baltimore). 2016;95:e4512. PMID 27512842. DOI: 10.1097/MD.0000000000004512
7. Morgan RL et al. Eradication of hepatitis C virus infection and the development of hepatocellular carcinoma. Ann Intern Med. 2013;158:329-337. PMID 23460056. DOI: 10.7326/0003-4819-158-5-201303050-00005
8. Younossi Z et al. Global burden of liver disease: 2023 update. J Hepatol. 2023;79:516-537. PMID 37236954. DOI: 10.1016/j.jhep.2023.03.017
9. Backus LI et al. A Sustained Virologic Response Reduces Risk of All-Cause Mortality in Patients With Hepatitis C. Clin Gastroenterol Hepatol. 2011;9:509-516. PMID 21397729. DOI: 10.1016/j.cgh.2011.03.004
10. AASLD/IDSA HCV Guidance Panel. Hepatitis C guidance 2018 update: AASLD-IDSA recommendations. Clin Infect Dis. 2018;67:1477-1492. PMID 30215672. DOI: 10.1093/cid/ciy585
11. US Preventive Services Task Force. Hepatitis C Virus Infection in Adolescents and Adults: Screening. JAMA. 2020;323:970-975. PMID 32119076. DOI: 10.1001/jama.2020.1366
12. Singal AG et al. AASLD practice guidance on prevention, diagnosis, and treatment of hepatocellular carcinoma. Hepatology. 2023;78:1922-1965. PMID 37199193. DOI: 10.1097/HEP.0000000000000466

PubMed Topic Searches

1. Hepatitis C DAA treatment outcomes
2. HCV cirrhosis surveillance
3. HCV extrahepatic manifestations
4. HCV SVR fibrosis regression
5. HCV global epidemiology
6. Hepatitis C screening guidelines

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Connections

• Gastroenterology
• Liver Cirrhosis
• Fatty Liver Disease (MASLD)
• Autoimmune Hepatitis
• Primary Biliary Cholangitis
• Esophageal Varices
• Hepatic Encephalopathy
• Portal Hypertension
• Cholangitis
• All Conditions
• Lab Tests
• Iron

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