• Chronic hepatitis C
• Direct-acting antiviral agents
• Hepatocellular carcinoma
• Liver-related events
• Taiwan hepatitis C virus registry

• Humans
• Taiwan/epidemiology
• Male
• Female
• Middle Aged
• Antiviral Agents/therapeutic use
• Hepatitis C, Chronic/drug therapy
• Hepatitis C, Chronic/epidemiology
• Liver Neoplasms/epidemiology
• Liver Neoplasms/virology
• Liver Neoplasms/prevention & control
• Sustained Virologic Response
• Carcinoma, Hepatocellular/epidemiology
• Carcinoma, Hepatocellular/prevention & control
• Carcinoma, Hepatocellular/virology
• Liver Cirrhosis/epidemiology
• Liver Cirrhosis/virology
• Adult
• Aged
• Ribavirin/therapeutic use
• Cohort Studies
• Registries
• Incidence
• Drug Therapy, Combination
• Proportional Hazards Models
• Treatment Outcome

• MOST111-2314-B-039-061-MY3 National Science and Technology Council

• Humans
• Liver Cirrhosis/genetics

• National Inpatient Sample
• direct-acting antiviral
• healthcare utilization
• hepatitis C
• hospitalization

• Adult
• Male
• Humans
• Aged
• United States/epidemiology
• Adolescent
• Hepacivirus
• Antiviral Agents/therapeutic use
• Medicare
• Hepatitis C, Chronic/drug therapy
• Hepatitis C/drug therapy
• Hepatitis C/epidemiology
• Hepatitis C/complications
• Hospitalization

• CC999999 Intramural CDC HHS

• Fibrosis
• HCV
• Longitudinal assessment
• Real-world
• Treatment failure

• AFP
• FIB-4
• MELD
• ascites
• cirrhosis
• gastrointestinal bleeding
• hepatitis C virus
• hepatocellular carcinoma
• predictor
• thrombocytopenia

• Humans
• Antiviral Agents/therapeutic use
• Carcinoma, Hepatocellular/drug therapy
• Hepacivirus
• Retrospective Studies
• Ascites/chemically induced
• Ascites/drug therapy
• Hepatitis C, Chronic/complications
• Hepatitis C, Chronic/drug therapy
• Hepatitis C/drug therapy
• Liver Cirrhosis/complications
• Liver Cirrhosis/drug therapy
• Liver Cirrhosis/epidemiology
• Liver Neoplasms/drug therapy
• Thrombocytopenia/complications
• Thrombocytopenia/drug therapy

To reach the WHO target of hepatitis C virus (HCV) elimination by 2025, Taiwan started to implement free-of-charge direct-acting antiviral (DAA) treatment programme in 2017. Evaluating the progress of HCV microelimination among people living with HIV (PLWH) is a critical step to identify the barriers to HCV elimination. PLWH seeking care at a major hospital designated for HIV care in Taiwan between January 2011 and December 2021 were retrospectively included. For PLWH with HCV-seropositive or HCV seroconversion during the study period, serial HCV RNA testing was performed using archived samples to confirm the presence of HCV viremia and estimate the prevalence and incidence of HCV viremia. Overall, 4199 PLWH contributed to a total of 27,258.75 person-years of follow-up (PYFU). With the reimbursement of DAAs and improvement of access to treatments, the prevalence of HCV viremia has declined from its peak of 6.21% (95% CI, 5.39–7.12%) in 2018 to 2.09% (95% CI, 1.60–2.77%) in 2021 (decline by 66.4% [95% CI, 55.4–74.7%]); the incidence has declined from 25.94 per 1000 PYFU (95% CI, 20.44–32.47) in 2019 to 12.15% per 1000 PYFU (95% CI, 8.14–17.44) (decline by 53.2% [95% CI, 27.3–70.6%]). However, the proportion of HCV reinfections continued to increase and accounted for 82.8% of incident HCV infections in 2021. We observed significant declines of HCV viremia among PLWH with the expansion of the DAA treatment programme in Taiwan. Further improvement of the access to DAA retreatments is warranted to achieve the goal of HCV microelimination.

• Men who have sex with men
• direct-acting antiviral
• injection drug use
• sexually transmitted disease
• sustained virologic response

• Men who have sex with men
• condomless receptive anal intercourse
• genotype switch
• phylogenetic analysis
• sexually transmitted disease

• epidemiology of viral hepatitis
• foetal outcome
• hepatitis A
• hepatitis B
• hepatitis C
• hepatitis D
• hepatitis E
• immunopathogenesis of viral hepatitis
• maternal transmission
• pathogenicity of viral hepatitis
• pregnancy
• viral hepatitis

• hcv
• direct-acting antivirals
• treatment failure
• machine learning

• Antiviral Agents/therapeutic use
• Carcinoma, Hepatocellular
• HIV Infections/drug therapy
• Hepacivirus
• Hepatitis C/drug therapy
• Hepatitis C, Chronic/epidemiology
• Humans
• Liver Cirrhosis
• Liver Neoplasms
• Spain/epidemiology

• exosomes
• liver disease
• role
• therapeutic potential

• Advances
• Future treatment
• Research
• Therapeutics
• Vaccines
• Viral hepatitis

• Antiviral Agents/therapeutic use
• Hepatitis A/epidemiology
• Hepatitis A/prevention & control
• Hepatitis B/diagnosis
• Hepatitis B/drug therapy
• Hepatitis B/prevention & control
• Hepatitis, Viral, Human/drug therapy
• Hepatitis, Viral, Human/epidemiology
• Hepatitis, Viral, Human/prevention & control
• Humans
• Liver Neoplasms/drug therapy

Patients with hepatitis C virus (HCV) frequently remain at risk for cirrhosis after sustained virologic response (SVR). Existing cirrhosis predictive models for HCV do not account for dynamic antiviral treatment status and are limited by fixed laboratory covariates and short follow up time. Advanced fibrosis assessment modalities, such as transient elastography, remain inaccessible in many settings. Improved cirrhosis predictive models are needed.

We developed a laboratory-based model to predict progression of liver disease after SVR. This prediction model used a time-varying covariates Cox model adapted to utilize longitudinal laboratory data and to account for antiretroviral treatment. Individuals were included if they had a history of detectable HCV RNA and at least 2 AST-to-platelet ratio index (APRI) scores available in the national Veterans Health Administration from 2000 to 2015, Observation time extended through January 2019. We excluded individuals with preexisting cirrhosis. Covariates included baseline patient characteristics and 16 time-varying laboratory predictors. SVR, defined as permanently undetectable HCV RNA after antiviral treatment, was modeled as a step function of time. Cirrhosis development was defined as two consecutive APRI scores > 2. We predicted cirrhosis development at 1-, 3-, and 5-years follow-up.

In a national sample of HCV patients (n = 182,772) with a mean follow-up of 6.32 years, 42% (n = 76,854) achieved SVR before 2016 and 16.2% (n = 29,566) subsequently developed cirrhosis. The model demonstrated good discrimination for predicting cirrhosis across all combinations of laboratory data windows and cirrhosis prediction intervals. AUROCs ranged from 0.781 to 0.815, with moderate sensitivity 0.703–0.749 and specificity 0.723–0.767.

A novel adaptation of time-varying covariates Cox modeling technique using longitudinal laboratory values and dynamic antiviral treatment status accurately predicts cirrhosis development at 1-, 3-, and 5-years among patients with HCV, with and without SVR. It improves upon earlier cirrhosis predictive models and has many potential population-based applications, especially in settings without transient elastography available.

The online version contains supplementary material available at 10.1186/s12911-021-01711-7.

• Hepatitis C virus
• Prediction
• Survival model
• Sustained virologic response
• Veterans

• Antiviral Agents/blood
• Antiviral Agents/pharmacokinetics
• Area Under Curve
• Carbamates/blood
• Carbamates/pharmacokinetics
• Cohort Studies
• Drug Therapy, Combination
• Female
• HIV Infections
• Hepatitis C, Chronic/drug therapy
• Humans
• Imidazoles/blood
• Imidazoles/pharmacokinetics
• Male
• Middle Aged
• Pilot Projects
• Prospective Studies
• Pyrrolidines/blood
• Pyrrolidines/pharmacokinetics
• Sofosbuvir/blood
• Sofosbuvir/pharmacokinetics
• Valine/analogs & derivatives
• Valine/blood
• Valine/pharmacokinetics

• T-COACH
• chronic hepatitis C
• decompensated liver disease
• hepatocellular carcinoma
• liver cirrhosis

• Decision tree analysis
• Linkage to care
• Random forest modeling
• Treatment initiation
• Virologic cure

• ACLD
• Ascites
• Cirrhosis
• Fibrosis
• Hepatic encephalopathy
• Inflammation
• Portal hypertension
• Variceal bleeding

• Ascites
• Esophageal and Gastric Varices
• Gastrointestinal Hemorrhage
• Humans
• Hypertension, Portal
• Liver Cirrhosis/complications

• Direct-Acting Antiviral
• Fibrosis Regression
• Hepatitis C Virus
• Sustained Virologic Response

• Animals
• Antiviral Agents/therapeutic use
• Hepacivirus/drug effects
• Hepacivirus/pathogenicity
• Hepatitis C/drug therapy
• Hepatitis C/metabolism
• Hepatitis C/pathology
• Hepatitis C/virology
• Host-Pathogen Interactions
• Humans
• Liver/drug effects
• Liver/metabolism
• Liver/pathology
• Liver/virology
• Liver Cirrhosis/drug therapy
• Liver Cirrhosis/metabolism
• Liver Cirrhosis/pathology
• Liver Cirrhosis/virology
• Liver Regeneration/drug effects
• Remission Induction
• Translational Research, Biomedical
• Treatment Outcome

• R01 DK056621 NIDDK NIH HHS
• P30 DK123704 NIDDK NIH HHS
• R01 DK098819 NIDDK NIH HHS
• P20 GM130457 NIGMS NIH HHS
• R01 DK128289 NIDDK NIH HHS
• R56 DK056621 NIDDK NIH HHS
• R01 DK113159 NIDDK NIH HHS
• R01 DK057830 NIDDK NIH HHS

The incidence of hepatocellular carcinoma (HCC) decreases significantly in chronic hepatitis C (CHC) patients with sustained virologic response (SVR) after pegylated-interferon plus ribavirin (PR) or direct-acting antiviral (DAAs) therapy. We follow-up a single cohort of CHC patients to identify risk factors associated with HCC development post-SVR.

CHC patients with SVR in Beijing/Hong Kong were followed up at 12–24 weekly intervals with surveillance for HCC by ultrasonography and alpha-fetoprotein (AFP). Multivariate Cox proportional hazards regression analysis was used to explore factors associated with HCC occurrence.

Between October 2015 and May 2017, SVR was observed in 519 and 817 CHC patients after DAAs and PR therapy respectively. After a median post -SVR follow-up of 48 months, HCC developed in 54 (4.4%) SVR subjects. By adjusted Cox analysis, older age (≥55 years) [HR 2.4, 95% CI (1.3–4.3)], non-alcoholic fatty liver diseases [HR 2.4, 95%CI (1.3–4.2), higher AFP level (≥20 ng/ml) [HR 3.4, 95%CI (2.0–5.8)], higher liver stiffness measurement (≥14.6 kPa) [HR 4.2, 95%CI (2.3–7.6)], diabetes mellitus [HR 4.2, 95%CI (2.4–7.4)] at pre-treatment were associated with HCC occurrence. HCC patients in the DAAs induced SVR group had a higher prevalence of NAFLD as compared with those in the PR induced SVR group, 62% (18/29) vs 28% (7/25), p = 0.026. A nomogram formulated with the above six independent variables had a Concordance-Index of 0.835 (95% CI 0.783–0.866).

Underlying NAFLD is associated with increased incidence of HCC in chronic HCV patients post-SVR, particularly in those treated with DAA.

•

Patients with chronic hepatitis C infection are still at risk of HCC after achieving sustained virus clearance (SVR).

• AFP, alpha-fetoprotein
• ALT, alanine aminotransferase
• ANGPTL, angiopoietin-like proteins
• AST, aspartate aminotransferase
• ASV, asunaprevir
• BCLC, Barcelona-Clinic Liver Cancer Group
• BMI, body mass index
• CHC, chronic hepatitis C
• CI, confidence intervals (CI)
• Chronic hepatitis C
• DAAs, direct-acting antiviral agents
• DCV, daclatasvir
• FGF, fibroblast growth factor
• HCC
• HCC, hepatocellular carcinoma
• HCV, hepatitis C virus
• HR, Hazard Ratio
• IFN, interferon
• LDV, ledipasvir
• LSM, liver stiffness measurement
• NAFLD
• PLT, platelet count
• PR, Peg-IFN-α with RBV
• Peg-IFN, Pegylated interferon
• RBV, ribavirin
• SMV, simeprevir
• SOF, sofosbuvir
• SVR, sustained virologic response
• Sustained virologic response
• TBIL, total bilirubin
• TNF, tumor necrosis factor
• ULN, upper limit of normal

• Aged
• Antiviral Agents/therapeutic use
• Comprehensive Health Care/methods
• Comprehensive Health Care/organization & administration
• Female
• Hepacivirus
• Hepatitis C/diagnosis
• Hepatitis C/drug therapy
• Hepatitis C/epidemiology
• Humans
• Male
• Mass Screening/methods
• Mass Screening/organization & administration
• Middle Aged
• Prospective Studies
• Quality Improvement
• Sustained Virologic Response
• United States/epidemiology
• Washington/epidemiology

• U51 PS004601 NCHHSTP CDC HHS
• Centers for Disease Control and Prevention

• Adolescent
• Adult
• Antiviral Agents/economics
• Antiviral Agents/therapeutic use
• Black People/statistics & numerical data
• Coinfection/drug therapy
• Female
• Florida/epidemiology
• HIV Infections/drug therapy
• HIV Infections/epidemiology
• Hepatitis C, Chronic/drug therapy
• Hepatitis C, Chronic/epidemiology
• Humans
• Male
• Medicaid/statistics & numerical data
• Middle Aged
• Patient Acceptance of Health Care/statistics & numerical data
• Proportional Hazards Models
• Retrospective Studies
• Substance-Related Disorders/complications
• United States
• White People/statistics & numerical data
• Young Adult
• Black or African American

• K01 DA045618 NIDA NIH HHS
• U24 AA022002 NIAAA NIH HHS
• National Institute on Drug Abuse
• National Institute on Alcohol Abuse and Alcoholism

• cirrhosis
• screening
• temporal trends
• viral hepatitis

Hepatitis C virus infection is a major cause of chronic hepatitis, leading to cirrhosis and hepatocellular carcinoma (HCC). Many studies agree that interferon (IFN)-based antiviral therapy can reduce the risk of HCC recurrence in patients with chronic hepatitis C who have achieved a sustained virological response (SVR). The recent introduction of direct-acting antivirals (DAA) has resulted in excitingly high SVR rates. However, as an IFN-free regimen, DAAs only exert antiviral activity without an immune response. The benefit of DAA-based regimens for HCC recurrence in patients with cirrhosis and following successful curative treatment remains controversial. Additionally, the time span between curative-intent therapy and the DAA regimen is an independent risk factor for HCC recurrence, irrespective of the DAA response. HCC patients who are eligible for potentially curative therapy by liver resection or ablation should defer DAA therapy; however, the accurate timing remains unclear. In this study, we reviewed the timing of DAA initiation after curative treatment and its effect on the recurrence of related HCC.

• DAA
• HCC
• HCV
• cirrhosis
• curative treatment
• recurrence

Hepatitis C virus (HCV) infection is increasing among pregnant women because of the opioid epidemic, yet there are no interventions to reduce perinatal HCV transmission or to treat HCV during pregnancy. Physiological changes in pregnancy alter the pharmacokinetics of some medications; thus, our aim was to compare the pharmacokinetic parameters of ledipasvir 90 mg plus sofosbuvir 400 mg during pregnancy with non-pregnant women.

This was an open-label, phase 1 study of pregnant women with genotype 1 HCV infection and their infants. A reference group of women who had participated in pharmacokinetic studies of ledipasvir–sofosbuvir during phase 2 and 3 trials was used. Participants were enrolled at Magee-Womens Hospital (Pittsburgh, PA, USA) between 23 and 24 weeks’ gestation and had a 12-week course of oral ledipasvir–sofosbuvir (daily 90 mg ledipasvir plus 400 mg sofosbuvir). Three 12-h intensive pharmacokinetic visits were done at 25–26, 29–30, and 33–34 weeks’ gestation and individual pharmacokinetics were summarised by geometric mean across the three visits. The primary outcome, analysed in all participants without suspected dosing errors, was the ledipasvir–sofosbuvir area under the concentration–time curve of the dosing interval (AUC_tau) during pregnancy compared with the reference group by geometric mean ratio. This study is registered with ClinicalTrials.gov, NCT02683005.

From Oct 1, 2016, to Sept 30, 2018, 29 pregnant women were screened and nine (31%) were enrolled. Eight (89%) women were included in the primary analysis. Ledipasvir and sofosbuvir exposures were similar in the pregnant women versus the non-pregnant reference group (geometric mean ratio of AUC_tau ledipasvir 89·3% [90% CI 68·7–116·1]; sofosbuvir 91·1% [78·0–106·3]).

Ledipasvir–sofosbuvir was safe and effective without clinically meaningful differences in drug exposure among pregnant versus non-pregnant women.

National Institutes of Health/Eunice Kennedy Shriver National Institute of Child Health and Human Development, the National Institutes of Health/Office of Research on Women’s Health, and Gilead Sciences.

• Antiviral therapy
• Extrahepatic manifestations
• Mortality
• Quality of life
• SVR
• Survival
• Sustained virologic response

• direct-acting antivirals
• hepatitis C
• response-guided therapy

• chronic HCV
• direct-acting antiviral
• sustained virologic response

• AbbVie 3D
• Direct acting anti-viral agents
• HCV
• Protease inhibitors failure

• hcv screening
• direct-acting antiviral treatment
• hcv guidance
• chronic hcv treatment

This study aimed to clarify the clinical picture of hepatitis C virus (HCV) carriers with normal alanine aminotransferase (CNALT) and those with ALT elevation (non‐CNALT) under direct‐acting antivirals (DAAs).

We enrolled 1002 patients with HCV (427 men, median age: 69 years) who had received DAAs for comparisons between CNALT (ALT ≤33 U/L in males and ≤25 U/L in females; n = 374) and non‐CNALT (n = 628) groups.

CNALT patients displayed a higher platelet count (PLT) (170 000 vs 146 000/μL, P < 0.0001) and albumin (4.1 vs 4.1 g/dL, P = 0.0006) but lower AST (25 vs 51 U/L, P < 0.0001), alpha fetoprotein (3.2 vs 5.4 ng/mL, P < 0.0001), and liver fibrosis marker scores (all P < 0.0001). The sustained virologic response rate was comparable between the CNALT and non‐CNALT groups (97.8 vs 95.3%, P = 0.106). The cumulative incidence of hepatocellular carcinoma (HCC) after DAA treatment was comparable between the CNALT and non‐CNALT groups (P = 0.117, log‐rank test). In CNALT patients with HCC history, PLT ≥150 000/μL was an independent risk factor of HCC recurrence (P = 0.019). In non‐CNALT patients without HCC history, male gender (P = 0.021) and albumin <4.0 g/dL (P = 0.007) were independent risk factors, while PLT < 150 000/μL (P = 0.081) was a marginal risk factor of HCC occurrence.

CNALT patients displayed a milder degree of liver fibrosis. Combinations of CNALT and PLT status might be useful as markers for HCC occurrence or recurrence surveillance.

• direct‐acting antiviral
• hepatitis C virus
• hepatitis C virus carrier with normal alanine aminotransferase
• hepatocellular carcinoma

• esophageal varices
• hepatocellular carcinoma
• liver cirrhosis
• mortality
• sustained virologic response

Patient: Male, 72

Final Diagnosis: Decompensated liver cirrhosis

Symptoms: Disturbance of consciousness

Medication: —

Clinical Procedure: PSE • BRTO • HCV treatment

Specialty: Radiology

• Direct-acting antiviral agent
• Hepatitis C virus
• Hepatocellular carcinoma
• Interferon-based therapy
• Recurrence

• Aged
• Antiviral Agents/administration & dosage
• Carcinoma, Hepatocellular/drug therapy
• Carcinoma, Hepatocellular/mortality
• Carcinoma, Hepatocellular/virology
• Female
• Follow-Up Studies
• Hepacivirus/drug effects
• Hepacivirus/isolation & purification
• Hepatitis C/complications
• Hepatitis C/drug therapy
• Hepatitis C/virology
• Humans
• Interferons/administration & dosage
• Liver Neoplasms/drug therapy
• Liver Neoplasms/mortality
• Liver Neoplasms/virology
• Male
• Middle Aged
• Neoplasm Recurrence, Local/drug therapy
• Neoplasm Recurrence, Local/mortality
• Neoplasm Recurrence, Local/virology
• Prognosis
• Retrospective Studies
• Survival Rate
• Sustained Virologic Response

Background: American Indian/Alaska Natives (AI/ANs) are disproportionately affected by hepatitis C virus (HCV), with more than double the national rate of HCV-related mortality as well as the highest rates of acute HCV. The “cascade of care” for HCV consists of screening, confirmation, treatment, and sustained virologic clearance (SVR)/cure. At each stage of this process, patients can be lost to follow-up. Federal health care facilities in an administrative area of the Indian Health Service conducted a review to identify and address gaps in HCV treatment. Facilities generally treated HCV with a strong pharmacy component using a collaborative practice agreement and HCV telehealth services to external specialists. Methods: All facilities had a pharmacist HCV program point of contact. Each pharmacist conducted a chart review of HCV patients and submitted aggregate results on HCV antibody status, HCV confirmation testing, stage of liver disease, initiation of treatment, and SVR/cure. Each facility also ranked current barriers to scaling up HCV treatment services from a defined list of options. Results: Of 1789 HCV antibody positive patients, 77% (1381) had a confirmation test, of which 67% (929) were positive. Of these patients, 62% (576) had their liver fibrosis scored, and 58% (335) had initiated treatment. Of patients with an SVR/cure test, all (274/274) were negative. Discussion: These data indicate that rural clinics can be successful providing HCV diagnosis and treatment. Pharmacists can play a key role in HCV clinical services. The outcomes of each step in the treatment process at the facility level can vary widely due to local factors. The barriers to HCV care that persist are nonclinical.

• American Indian/Alaska Native
• access to care
• hepatitis C virus
• rural

Chronic liver disease (CLD) is a condition that progresses over time toward advanced disease state which is known as liver cirrhosis. Liver cirrhosis leads to dangerous health problems among people living across the world. One such problem that observed in about 75% of cirrhotic patients is thrombocytopenia; which in turn associated with poor prognosis and recovery from CLD. Beyond these, thrombocytopenia in cirrhotic patients led to impairment of coagulation cascade and significantly influenced the utilization of effective mechanism in the management of CLD. By nature, treatment of CLD involves invasive diagnostic and treatment procedures; therefore, in the presence of thrombocytopenia implementing these methods put the lives of patients in a critical health problem due to increased risk of bleeding and mortality. Because of these reasons, prophylactic transfusion of platelets is considered to be one of the most effective options that reduce the risk of bleeding in patients with CLD that required to undergo an invasive procedure. Although platelet transfusion presented with significant advantages in facilitating the invasive procedure in patients with CLD, refractoriness with repeated use and various problems associated with its transfusion limit the continuous utilization of this important option. With these challenges and current advance in the knowledge of thrombopoiesis, the development of relatively safe and alternative drugs that enhance the production of platelets by interacting with thrombopoietin receptor agonists provides a promising option to platelet transfusion. The discovery and approval of romiplostim and eltrombopag in August 2008 and November 2008, respectively, for the treatment of chronic immune thrombocytopenia paved a way and followed by the Food and Drug Administration (FDA) approval of 2 potentially advantageous drugs, lusutrombopag, and avatrombopag, in 2018 for the treatment of thrombocytopenia in patients with CLD that required to undergo elective surgery. Therefore, this review aims to assess pathogenesis of thrombocytopenia and its challenges in the management of liver-related issues and, more importantly, gives emphasis to address the potential use of avatrombopag in the treatment of thrombocytopenia underlying CLD, its pharmacokinetics and pharmacodynamics, as well as its toxicological profiles by presenting the most commonly reported adverse events in various trials.

• Thrombocytopenia
• avatrombopag
• chronic liver disease
• platelets
• thrombopoietin receptor agonists

• exosomes
• fibrosis
• hepatic stellate cells
• hepatitis C virus
• non-coding RNAs

• Carcinoma, Hepatocellular/pathology
• Carcinoma, Hepatocellular/virology
• Chemokines/metabolism
• Cytokines/metabolism
• Exosomes/metabolism
• Hepacivirus/metabolism
• Hepacivirus/pathogenicity
• Hepacivirus/physiology
• Hepatic Stellate Cells/metabolism
• Hepatitis C/drug therapy
• Hepatitis C/pathology
• Hepatitis C/virology
• Hepatitis C, Chronic/drug therapy
• Hepatitis C, Chronic/pathology
• Hepatitis C, Chronic/virology
• Hepatocytes/metabolism
• Humans
• Liver Cirrhosis/drug therapy
• Liver Cirrhosis/pathology
• Liver Cirrhosis/virology
• Liver Neoplasms/pathology
• Liver Neoplasms/virology

• R01 DK080812 NIDDK NIH HHS
• R01 DK113645 NIDDK NIH HHS
• R01 DK081817 NIDDK NIH HHS