Hepatitis C Management

Last updated: 30 March 2026
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Evaluation

General Care  

For supportive care, consider hospitalization and expert referral if there is vomiting, dehydration or signs of hepatic decompensation. Evaluate for advanced fibrosis or other conditions that may hasten liver fibrosis (eg HBV and HIV infections, genotype 3, metabolic dysfunction-associated steatotic liver disease [MASLD]) to help guide the treatment. Monitor for hepatocellular carcinoma with alpha-fetoprotein (AFP) and liver ultrasound every 6 months in those with advanced fibrosis. Screen for other sexually transmitted diseases in cases of sexually acquired hepatitis or if otherwise appropriate. Identify extrahepatic manifestations and treat comorbidities appropriately. Test for HIV infection, past or current HBV infection, and for HAV immunity, and search for other causes of liver comorbidities. 

Clinical Decision  

Antiviral therapy is currently widely accepted for the following hepatitis C patient groups:  ≥18 years of age, elevated serum alanine aminotransferase (ALT) levels, liver biopsy showing chronic hepatitis with significant fibrosis or cirrhosis (stage F1 or above), HCV genotype 2 or 3 regardless of stage, compensated liver disease, acceptable hematological and biochemical indices, and those who are willing to be treated and conform to patient requirements.  

Therapy should be individualized in patients with any of the following: Failed prior treatment of either Interferon given alone or in combination with Ribavirin or Peginterferon given alone; current alcoholic or person who injects drugs (PWID) but willing to participate in an alcohol support program or substance abuse program; acute hepatitis C; co-infected with HIV; individuals <18 years of age; chronic renal disease; known hypersensitivity to drugs used to treat HCV; decompensated cirrhosis; liver transplant recipient; pregnant (with careful maternal and fetal safety assessment) or unwilling/unable to comply with adequate contraception; severe concurrent disease (eg hypertension, heart failure, diabetes mellitus [DM], etc); and hepatic decompensation.

Factors to be Considered Before Treatment Initiation  

The factors to be considered before treatment initiation are the history of prior treatment and response to previous treatment; stage of fibrosis; HCV genotype, especially in patients with known cirrhosis or relapse after antiviral therapy; and comorbidities that may affect therapy.  

Factors Associated with Accelerated Fibrosis Progression  

The non-modifiable host factors associated with accelerated fibrosis progression are the fibrosis stage, inflammation grade, male sex, older age at the time of infection, and organ transplant. The modifiable host factors associated with accelerated fibrosis progression are alcohol consumption, insulin resistance, MASLD, and obesity. The viral factors are co-infection with HBV or HIV and genotype 3.

Principles of Therapy

Goals of Treatment  

The goals of therapy include the following: 

  •  The clinical objective of treatment of hepatitis C is to achieve virologic cure (sustained virologic response [SVR]) and eradication of HCV infection
  • Antiviral treatment for acute hepatitis C aims to prevent progression to chronic hepatitis C
  • Antiviral treatment of chronic hepatitis C aims to prevent the occurrence of liver-related complications (eg liver cirrhosis and hepatocellular carcinoma), development of extrahepatic manifestations (eg B cell lymphoma, essential mixed cryoglobulinemia, leukocytic vasculitis, membranoproliferative glomerulonephritis, neuropathy, porphyria cutanea tarda, renal disease) and HCV-related mortality
    • HCV therapy reduces the decompensation rate and hepatocellular carcinoma risk in patients with cirrhosis
    • Direct-acting antiviral therapy is recommended to improve survival in patients with cured HCV-related hepatocellular carcinoma
  • HCV therapy reduces the risk of cardiovascular disease (CVD), diabetes mellitus and insulin resistance
  • The prevention of transmission of HCV is also a goal of treatment

Principles of Treatment



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Treatment with antiviral therapy is indicated for all patients with acute or chronic hepatitis C without complications to treatment and both treatment-naive and treatment-experienced patients with compensated or decompensated cirrhosis. Treatment-naive patients are those who have never been treated for HCV infection. Treatment-experienced patients are those who were previously treated with Interferon or Peginterferon with or without Ribavirin, or Sofosbuvir plus Ribavirin with or without Peginterferon. Treatment should be prioritized for patients with advanced liver disease (fibrosis stage ≥F2 or cirrhosis), those with severe HCV-related extrahepatic manifestations, individuals awaiting or having undergone liver transplantation or populations at high risk of HCV transmission. Antiviral therapy is generally not recommended in patients with short or limited life expectancy that cannot be resolved with HCV therapy, liver transplantation, or other directed therapy, including those with non-liver related comorbidities who are not transplant candidates and are unlikely to derive clinical benefit from viral eradication. Interferon-free, Ribavirin-free, direct-acting antiviral-based regimens are the recommended treatment options: NS3/4A (protease) inhibitors such as Asunaprevir, Glecaprevir, Grazoprevir, Paritaprevir, Voxilaprevir; NS5A inhibitors such as Daclatasvir, Elbasvir, Ledipasvir, Ombitasvir, Pibrentasvir, Ravidasvir, Velpatasvir; NS5B polymerase inhibitor (nucleotide analogue) such as Sofosbuvir; and NS5B polymerase inhibitor (non-nucleoside analogue) such as Dasabuvir. 

The choice, course, and duration of therapy are influenced by the HCV genotype as well as the severity of liver disease, which must both be identified before starting treatment. Patients with confirmed hepatitis C should be treated with direct-acting antivirals without awaiting spontaneous resolution. HCV genotyping should be considered in patients with cirrhosis. In areas where virological tests are unavailable or are costly, or to simplify therapeutic regimen, pangenotypic therapy may be considered. Pangenotypic direct-acting antivirals are associated with shorter treatment durations, improved tolerability and SVR rates >95%, regardless of genotype. Comprehensive pretreatment evaluation of factors that may influence the treatment process or outcomes should be performed: Comorbid liver diseases, hepatocellular carcinoma, HBV co-infection, MASLD, alcohol-related liver disease, autoimmune hepatitis, pregnancy, and reinfection risk factors. Assess the risk for a drug-drug interaction before starting HCV therapy or other medications during therapy in patients receiving direct-acting antivirals and monitor for side effects during treatment. Patients initiating direct-acting antiviral therapy should also be assessed for HBV or HIV co-infection. Routine pretreatment resistance-associated substitution (RAS) testing is not recommended when pangenotypic direct-acting antiviral regimens are used; assessment for RAS should be considered in specific scenarios (eg certain genotype-specific regimens, prior direct-acting antiviral treatment failure). 

Treatment responses are usually characterized by HCV RNA testing. It is not recommended to routinely monitor HCV RNA during direct-acting antiviral therapy in patients with good adherence. Eradication of infection is considered when there is SVR. SVR is defined as the absence of HCV RNA in serum or plasma by a sensitive test at least 12 weeks after completing treatment. If HCV RNA assays are unavailable, an undetectable HCV core antigen in serum or plasma 24 weeks after completing treatment can be an alternative endpoint of therapy. Virological responses in patients with HCV infection treated with Interferon-based therapy can be defined as follows: Rapid virologic response (RVR) is achieved when HCV RNA becomes undetectable (<50 IU/mL) in serum after 4 weeks of therapy; early virologic response (EVR) is defined as a 2-log drop or loss of HCV RNA 12 weeks into therapy; and patients in whom HCV RNA levels remain stable while on treatment are considered non-responders, while those whose HCV RNA levels decline but never become undetectable are referred to as partial responders. 

End of treatment response is defined as continued absence of detectable virus at end of treatment. Recurrent HCV infection after therapy may result from either relapse or reinfection. Relapse is defined as reappearance of HCV RNA after treatment cessation in a patient whose HCV RNA became undetectable on therapy; it represents reactivation of the original virus, typically occurring within 4-12 weeks after treatment completion and resulting in failure to maintain SVR. Reinfection is defined as new viral acquisition after achieving SVR, characterized by reappearance of HCV RNA or HCV core antigen at any time after an SVR, usually in patients with ongoing high-risk behaviors. The detection of a different HCV genotype or a distinct strain compared with the pretreatment virus supports the diagnosis of reinfection rather than relapse. It must be noted that when relapse cannot be reliably differentiated from reinfection, it is advisable to manage the case as relapse and initiate retreatment with a salvage regimen that provides a high barrier to resistance.

Individualize treatment based on the following: Severity of liver disease, previous therapy, potential of serious side effects or drug-drug interactions with concomitant medications, likelihood of treatment response, and presence of comorbid conditions (in patients with HIV/HCV co-infection, antiretroviral therapy [ART] is suggested to be initiated first before direct-acting antiviral, however, if the patient is ineligible for ART, direct-acting antiviral can be initiated if there are no contraindications; in patients with HBV/HCV co-infection, HBV and HCV should be treated independently or concurrently according to monoinfection guidelines, with close monitoring for HBV reactivation during and after direct-acting antiviral therapy and prompt initiation of anti-HBV treatment if reactivation occurs.  in patients with hemoglobinopathies, the European Association for the Study of Liver [EASL] guidelines recommend direct-acting antiviral for HCV infection; patients with HCV-associated cryoglobulinemia should be treated with direct-acting antiviral; and patients with renal impairment [eGFR <30 mL/min/1.73 m2] or those on hemodialysis, Sofosbuvir-free treatment regimen is preferred). 

Recommended Management of Direct-acting Antiviral Treatment Interruptions for Treatment-Naive Patients

Interruptions before receiving 28 days of direct-acting antiviral therapy should be done in the following: When patients missed ≤7 days of treatment, direct-acting antiviral therapy is restarted immediately and must be completed for a planned duration of 8-12 weeks; and when patients missed ≥8 days of treatment, direct-acting antiviral therapy is restarted immediately and an HCV RNA test must be obtained as soon as possible preferably on the same day as therapy is restarted. HCV RNA-negative patients should complete the original planned duration of therapy (8-12 weeks). HCV RNA-negative patients with genotype 3 and/or with compensated cirrhosis and HCV RNA-positive patients (>25 IU/L) or if not obtained should extend direct-acting antiviral treatment for an additional 4 weeks from the original planned duration of therapy.  

Interruptions after receiving ≥28 days of direct-acting antiviral therapy should be done in the following: When patients missed ≤7 days of treatment, direct-acting antiviral therapy is restarted immediately and must be completed for a planned duration of 8-12 weeks; when patients missed 8-20 consecutive days of treatment, direct-acting antiviral therapy is restarted immediately and an HCV RNA test must be obtained as soon as possible preferably on the same day as therapy is restarted. HCV RNA-negative patients should complete the original planned duration of therapy (8-12 weeks). HCV RNA-negative patients with genotype 3 and/or with compensated cirrhosis should extend direct-acting antiviral treatment for an additional 4 weeks from the original planned duration of therapy. HCV RNA-positive patients (>25 IU/L) or if not obtained should stop treatment and treatment should be restarted. Interruptions after receiving ≥28 days of direct-acting antiviral therapy should also be done when patients missed ≥21 consecutive days of treatment; direct-acting antiviral therapy should be stopped SVR12 should be assessed. Retreatment is recommended in patients who have not achieved SVR12.  

Spontaneous Resolution in Acute Infection  

Patients with acute hepatitis C should be treated according to the simplified approach without awaiting spontaneous resolution. Patient education focusing on the reduction of viral transmission should be done. The chance of spontaneous resolution is greater in female patients and those with HCV genotype non-1 infection. This is less likely to happen if infection lasts >12 weeks.

Pharmacological therapy

Acute Hepatitis C  

The treatment for acute hepatitis C may be delayed for 8-12 weeks as there is a 20-50% chance of spontaneous resolution. Consider pharmacotherapy to prevent progression to chronic hepatitis C or to minimize transmission or loss to follow-up. Direct-acting antiviral therapy was shown to be cost-effective and improved clinical outcomes in comparison to delaying treatment until the chronic phase. Measure HCV RNA prior to starting therapy and SVR at 12 and 24 weeks after therapy.  

Pending further data that will establish the start time of the ideal treatment regimen and its duration, acute hepatitis C patients may be treated with the following antiviral regimens: Sofosbuvir/Velpatasvir for 12 weeks (all genotypes); Glecaprevir/Pibrentasvir for 8 weeks (all genotypes); Sofosbuvir/Ledipasvir for 8-12 weeks (genotypes 1, 4, 5 and 6); and Grazoprevir/Elbasvir for 12 weeks (genotypes 1b and 4). Interferon (high-dose) or Peginterferon may also be used. Treat HCV genotype 1 for 24 weeks, and genotype 2, 3, or 4 for 12 weeks. Patients who are unresponsive to monotherapy should be given Peginterferon/Ribavirin or a protease inhibitor-based triple therapy.  

Chronic Hepatitis C  
 
Patients with any of the following are eligible for the simplified pangenotypic HCV treatment: Chronic HCV infection, including persons living with HIV with infection of any genotype, without previous HCV treatment, and without cirrhosis or with compensated cirrhosis (Child-Pugh A).  

Patients with any of the following are ineligible for the simplified pangenotypic HCV treatment: HBsAg-positive; previous hepatitis C treatment; current or prior episode of decompensated cirrhosis; current pregnancy; known hepatocellular carcinoma; prior liver transplantation; and compensated liver cirrhosis with end-stage renal disease (eGFR <30 mL/min/1.73 m2).  

The recommended regimens are the following:

  • Treatment-naïve adults without cirrhosis:
    • Glecaprevir/Pibrentasvir for 8 weeks (all genotypes)
    • Sofosbuvir/Velpatasvir for 12 weeks (all genotypes)
  • Treatment-naïve adults with compensated cirrhosis:
    • Glecaprevir/Pibrentasvir for 8 weeks (all genotypes)
    • Sofosbuvir/Velpatasvir for 12 weeks (all genotypes except genotype 3) 


Genotype-specific Therapy  

Identify the HCV genotype and genotype 1 subtype (eg 1a or 1b) before initiating treatment to determine the choice and duration of therapy. The genotype and subtype should be determined in areas or settings where subtypes of HCV are resistant to NS5A inhibitors (eg subtypes 1l, 3b, 3g, 4r, 6u, 6v).

Regimen Genotype Treatment Experience Duration (weeks)
Daclatasvir plus Sofosbuvir with or without weight-based Ribavirin 1a, 1b Treatment-naive and treatment experienced, without cirrhosis   12-24
2, 3 Treatment-naive without cirrhosis or with compensated cirrhosis, treatment experienced without cirrhosis 24
Elbasvir/Grazoprevir  1a, 1b, 4 Treatment-naive, without cirrhosis or with compensated cirrhosis   12 
Glecaprevir/Pibrentasvir 1a, 1b, 2, 3, 4, 5, 6 Treatment-naive without cirrhosis or with compensated cirrhosis 8
1a, 1b, 2, 3, 4, 5, 6 Treatment-naive without cirrhosis or with compensated cirrhosis if co-infection of HIV/HCV is present 12
Ledipasvir/Sofosbuvir 1a, 1b, 4, 5, 6 (except 6e)
 Treatment-naive, without cirrhosis or with compensated cirrhosis 12
1a, 1b, 4, 5, 6  Treatment-naive with decompensated cirrhosis who are not qualified for Ribavirin therapy 24 
Ledipasvir/Sofosbuvir with weight-based Ribavirin 1a, 1b, 4, 5, 6  Treatment-naive with decompensated cirrhosis 12 
Sofosbuvir/Velpatasvir   1a, 1b, 2, 3*, 4, 5, 6 Treatment-naive, without cirrhosis or with compensated cirrhosis
 12
1a, 1b, 2, 3, 4, 5, 6  Treatment-naive with decompensated cirrhosis who are not qualified for Ribavirin therapy 24
Sofosbuvir/Velpatasvir with weight-based Ribavirin 3* Treatment-naive, with compensated cirrhosis and baseline NS5A Y93 RAS 12 
1a, 1b, 2, 3, 4, 5, 6  Treatment-naive with decompensated cirrhosis 12 
Sofosbuvir/Velpatasvir/Voxilaprevir  3* Treatment-naive and PEG/RBV experienced, with compensated cirrhosis and baseline NS5 Y93 RAS
 12
*If resistance testing is performed at baseline, patients with NS5A Y93H RAS for Velpatasvir should be treated with Sofosbuvir/Velpatasvir/Voxilaprevir or Sofosbuvir/Velpatasvir plus Ribavirin for 12 weeks; patients without the Y93H RAS should be treated with Sofosbuvir/Velpatasvir only for 12 weeks.
References: Bhattacharya D, Aronsohn A, Price J, et al. Hepatitis C guidance 2023 update: American Association for the Study of Liver Diseases – Infectious Diseases Society of America recommendations for testing, managing, and treating hepatitis C virus infection. Clin Infect Dis. 2023 May:ciad319; European Association for the Study of the Liver (EASL). EASL recommendations on treatment of hepatitis C. 2020.

Retreatment for Patients with Failure of Prior Therapy



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When planning retreatment for a patient who has failed previous HCV therapy, the retreatment regimen should be guided by a review of potential contributing factors to treatment failure, which should be identified and addressed prior to and during retreatment: Patient-related factors (eg poor adherence, presence of cirrhosis or impaired liver function, comorbidities), viral factors (eg HCV genotype [particularly genotype 3], RAS), and drug-related factors (eg drug–drug interactions, inadequate treatment duration, use of regimens with a low genetic barrier to resistance). Current standard salvage regimens have a high barrier to resistance, and the presence of RAS does not appear to significantly affect retreatment success rates.

Sofosbuvir-based treatment failure without cirrhosis or with compensated cirrhosis: Sofosbuvir/Velpatasvir/Voxilaprevir for 12 weeks for genotypes 1, 2, 4, 5, and 6, and patients with genotype 3 infection without cirrhosis. An addition of weight-based Ribavirin is recommended in patients with genotype 3 infection with compensated cirrhosis. If Ribavirin is contraindicated, consider extending treatment duration to 24 weeks. Glecaprevir/Pibrentasvir for 16 weeks as an alternative regimen for genotypes 1, 2, 4, 5 and 6. This is not recommended in patients with previous exposure to an NS5A inhibitor plus HCV non-structural protein 3-4a (NS3/4A) protease inhibitor regimen (eg Elbasvir/Grazoprevir).

Glecaprevir/Pibrentasvir treatment failure without cirrhosis or with compensated cirrhosis: Glecaprevir/Pibrentasvir plus Sofosbuvir and weight-based Ribavirin for 16 weeks for all genotypes. Sofosbuvir/Velpatasvir/Voxilaprevir for 12 weeks for all genotypes without cirrhosis. An addition of weight-based Ribavirin is recommended in patients with genotype 3 infection or with compensated cirrhosis. If Ribavirin is contraindicated, consider extending treatment duration to 24 weeks. 

Sofosbuvir/Velpatasvir/Voxilaprevir or Sofosbuvir plus Glecaprevir/Pibrentasvir treatment failure without cirrhosis or with compensated cirrhosis: Glecaprevir/Pibrentasvir plus Sofosbuvir and weight-based Ribavirin for 16 weeks for all genotypes. The treatment duration should be extended to 24 weeks in extremely difficult cases (eg genotype 3 with compensated cirrhosis) or in patients with treatment failure under Sofosbuvir plus Glecaprevir/Pibrentasvir therapy. Sofosbuvir/Velpatasvir/Voxilaprevir plus weight-based Ribavirin for 24 weeks for all genotypes.  

Peginterferon and Ribavirin with or without protease inhibitor treatment failure: Glecaprevir/Pibrentasvir for 16 weeks for genotype 3. Sofosbuvir/Velpatasvir for 12 weeks for patients with genotype 3 without cirrhosis and who do not have a Y93H variant. An addition of weight-based Ribavirin for 12 weeks is an alternative for patients with genotype 3 with compensated cirrhosis or Y93H variant. Sofosbuvir/Velpatasvir/Voxilaprevir for 12 weeks for patients with genotype 3 with compensated cirrhosis or Y93H variant. Sofosbuvir/Velpatasvir for 12 weeks in patients with genotypes 1, 2, 4, 5 or 6 and with or without compensated cirrhosis. Glecaprevir/Pibrentasvir for 8 weeks in patients with genotypes 1, 2, 4, 5 or 6 and without cirrhosis or protease inhibitor exposure. Administered for 12 weeks in patients with genotypes 1, 2, 4, 5 or 6 and with either cirrhosis or protease inhibitor exposure.  

Decompensated Cirrhosis  

Decompensated cirrhosis presents with ≥ 1 complications of portal hypertension such as variceal bleeding, ascites, jaundice or hepatic encephalopathy. Patients with genotypes 1-6 with decompensated cirrhosis and those with compensated cirrhosis with prior decompensation episodes should receive Sofosbuvir/Velpatasvir with weight-based Ribavirin for 12 weeks. Ribavirin can be initiated at 600 mg/day (200 mg/day in patients with severe renal impairment) with subsequent dose adjustments based on the patient's tolerance. If the patient has contraindications to or is intolerant of Ribavirin, Sofosbuvir/Velpatasvir alone can be given for 24 weeks. Sofosbuvir/Velpatasvir with weight-based Ribavirin for 24 weeks is recommended as retreatment for patients with genotypes 1-6 with decompensated cirrhosis who failed treatment with a direct-acting antiviral (protease inhibitor and/or NS5A inhibitor)-containing regimen. Treatment regimens that include a HCV protease inhibitor (eg Glecaprevir, Grazoprevir or Voxilaprevir) or Interferon-based regimens should not be given. 

HCV Genotype 1, 4, 5 or 6  

Those with decompensated cirrhosis who are Ribavirin eligible may take Ledipasvir/Sofosbuvir with low initial dose of Ribavirin (may be increased as tolerated) for 12 weeks. Those with decompensated cirrhosis who are Ribavirin ineligible may take Ledipasvir/Sofosbuvir for 24 weeks or Sofosbuvir/Velpatasvir for 12 weeks for genotype 1. Those with decompensated cirrhosis and in whom previous Sofosbuvir- or NS5A-based treatment has failed may take Ledipasvir/Sofosbuvir with low initial dose of Ribavirin (may be increased as tolerated) for 24 weeks.  

HCV Genotype 2 or 3  

Those with decompensated cirrhosis who are Ribavirin ineligible may take Sofosbuvir/Daclatasvir or Sofosbuvir/Velpatasvir for 24 weeks, and Sofosbuvir/Velpatasvir for 12 weeks for genotype 2.

Nonpharmacological

Patient Education



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Provide the patients with a detailed explanation of their condition. Emphasize the disease's long-term implications (eg long-term medical therapy, continuous monitoring for liver disease progression) for their and their partners' health. Counsel regarding the importance of treatment adherence, proper dosing administration, and reporting of medication changes. Provide a clear, accurate, and written information.  Advise the patient not to donate blood, semen or organs. Advise the patient to avoid sharing items of personal hygiene (eg toothbrushes, shaving equipment, razors, nail clippers). Counsel the patient to stop illicit drug use and unsafe injection practices, and to never reuse, share or improperly dispose injection equipment. Advise the patient regarding sexual transmission. HCV is not considered to be a sexually transmitted disease, but sexual promiscuity, HIV and herpes simplex virus (HSV-2) co-infections are associated with sexual transmission of hepatitis C. Consistent condom use is recommended for individuals with multiple sexual partners and unprotected sex is avoided during menstruation. Immediately after exposure to HCV-infected blood or body fluids, baseline anti-HCV and ALT are obtained; if anti-HCV is negative, HCV RNA testing is performed at 4-6 weeks after exposure for early detection, and if all baseline tests are negative, anti-HCV and ALT are repeated at 4-6 months after exposure. Advise the patient regarding the potential deleterious effect of alcohol especially in association with the development of hepatocellular carcinoma, the progression of liver fibrosis, and the increase in HCV replication. Breastfeeding is considered safe for mothers with hepatitis C unless there is nipple injury or bleeding, in which case feeding from the affected breast should be avoided.  

Partner Notification  

Notify the partner for at-risk contacts. Contact tracing to include any sexual contact (penetrative vaginal or anal sex) or needle-sharing partners from 2 weeks before the onset of jaundice. If without acute infection, trace back to the likely time of infection (eg blood transfusion, first needle sharing).

Surgery

Liver Transplantation  

Liver transplantation is indicated in patients with end-stage liver disease (decompensated cirrhosis), hepatocellular carcinoma, and acute liver failure (ie caused by viruses, drugs and toxic agents). This is considered in patients with expected survival of ≤1 year without transplantation or if quality of life is unsatisfactory due to liver disease. Patients with HCV infection can be treated prior to or after transplant on a case-by-case basis. In patients with chronic HCV infection awaiting liver transplantation or with advanced hepatic impairment, direct-acting antiviral therapy is recommended to improve liver function and prevent post-transplant recurrence, with careful monitoring for adverse effects and treatment-related toxicity. When transplantation is not possible due to limited access or availability, direct-acting antiviral therapy may be considered in patients who are likely to have liver function improvement. For patients likely to undergo liver transplantation within 3 months, prioritize transplant and defer antiviral therapy until post-transplant if HCV recurs. If there is hepatitis C recurrence post-transplant, treatment with antivirals is prioritized and is started early in patients with significant graft damage. A 12-week course of Sofosbuvir/Velpatasvir or Glecaprevir/Pibrentasvir is recommended. In transplant recipients, direct-acting antiviral therapy is initiated after the immunosuppressive regimen has been stabilized, if clinically feasible. HCV replication is not a contraindication for liver transplantation, though antiviral therapy should be given after transplant.

Prevention

Primary Prevention  

At present, there is no available vaccine for the HCV. The prevention of HCV would depend on the reduction of the risk of exposure especially in patients in healthcare settings and those who are in a high-risk population (eg IV drug use and through sexual contact). The HCV RNA should be assessed at 6 or 12 months after SVR to monitor for HCV reinfection in the high-risk population. 

The recommended primary interventions are: Hand hygiene should include proper surgical hand preparation, hand washing and use of gloves; appropriate and safe use of healthcare injection; proper handling and disposal of sharp needles and other objects and waste; comprehensive harm-reduction services should be provided to persons who injects drugs including the use of sterile injecting equipment and treatment of dependence; single use or sterilization of equipment; all healthcare personnel should be trained and healthcare facilities must strictly follow standard precautions for all procedures with potential blood exposure; donated blood should be tested for HBV, HCV, HIV, and syphilis; and proper and consistent use of condoms should be promoted.



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Secondary and Tertiary Prevention  

Secondary and tertiary prevention recommendations for people who are infected with HCV: Conduct an education and counseling program for patient care and treatment, including the risk of reinfection and prevention of HCV transmission; immunization with hepatitis A and B vaccines is recommended to prevent co-infection and provide protection to the liver; early and appropriate medical management including the use of antiviral therapy; and routine laboratory, therapeutic and toxicity monitoring can be limited at the start and end of antiviral treatment. An HCV RNA 12 weeks post-direct-acting antiviral can be used to assess SVR; HCV core antigen 24 weeks post-direct-acting antiviral can be an alternative. LFTs and serum creatinine can be done during week 4 of antiviral therapy and 12 weeks post-treatment. CBC monitoring should be done in patients treated with Ribavirin. Regular monitoring is the key to early diagnosis of chronic liver disease. Patients with advanced fibrosis or cirrhosis should continue hepatocellular carcinoma surveillance every 6 months and be monitored for cirrhosis-related complications even after achieving SVR, as SVR reduces but does not eliminate the risk of hepatocellular carcinoma. 

Post-SVR risk factor management: Patients at high risk for HCV reinfection should undergo periodic HCV RNA monitoring after achieving SVR. Patients with persistent excessive alcohol use or coexisting MASLD should continue to receive management of these risk factors after achieving SVR. Lastly, patients who do not achieve SVR should be managed in the same manner as those with chronic hepatitis C or cirrhosis.