Interleukin-28B (IL-28B) and Interferon –Gamma (INF-γ) Levels in Patients with Chronic Hepatitis C Viral (HCV) Infection

Objectives: We aimed to studythe effect of Schsitosoma mansoni co-infection with hepatitis C virus (HCV) on IL-28B levels. Design: We collected plasma from107outpatients(range30–81 years old) from six governates of Delta, Egypt attending Kasr Al-Aini Hospital, Cairo, Egyptin 2012–2014. Subjects were divided to three groups, 35 healthy controls, 50naïve chronic HCV patientsand 22S. mansoni/HCVco-infected patients.For all participants,anti-schistosomal antibodies levels, hepatitis B surface antigens (HBsAg), HCV viral loadand routine liver function tests were measured. We assayed IL-28B and IFN-γ plasma levels for all participants. Results: We found that IL-28B levelsweresignificantly higher in S. mansoni/HCV co-infected patients than in HCV mono-infection. IFN-γ and IL-28B levels showed positive correlation in both infected groups. Patients with high HCV viral load had significantly higher IFN-γ and IL-28B levelswhether suffering from mono- or co-infection. Conclusions: A strong link between IFN-γ and IL-28B in naïve chronic HCV patients whether mono- or co-infected with S. mansoni. This suggeststhat co-infection with S. mansoni might not affect IFN-γ levels, however, significantly increases IL-28B levels. Therefore, IL-28B plasma levels might be a useful novel biomarker forprognosis and therapy ofS. mansoni/HCV co-infection

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Genetic polymorphisms as the predictors of response to antiviral treatment in chronic hepatitis C virus infection

Orvosi Hetilap ◽

10.1556/oh.2011.29113 ◽

2011 ◽

Vol 152 (22) ◽

pp. 876-881

Author(s):

Alajos Pár

Keyword(s):

Chronic Hepatitis ◽

Hepatitis C Virus ◽

Hepatitis C ◽

Genetic Polymorphisms ◽

Chronic Hepatitis C ◽

Genome Wide Association Study ◽

Antiviral Treatment ◽

Hcv Infection ◽

Snp Analysis ◽

Chronic Hcv

The review discusses the genetic polymorphisms involved in the pathogenesis of hepatitis C virus (HCV) infection, that may determine the outcome of disease. In this field earlier both certain major histocompatibility complex (MHC) alleles and some cytokine gene variants have also been studied. Recently, the genome-wide association study (GWAS) and targeted single nucleotide polymorphism (SNP) analysis have revealed that a variant in the promoter region of interleukin-28B (IL-28B) gene is strongly linked to viral clearance and it may be the strongest pretreatment predictor of treatment response in chronic hepatitis C. Last year it was shown that two genetic variants leading to inosine triphosphatase deficiency protect against haemolytic anemia in patients receiving ribavirin during antiviral treatment for chronic HCV infection. Orv. Hetil., 2011, 152, 876–881.

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Faculty Opinions recommendation of Quantitative liver function tests improve the prediction of clinical outcomes in chronic hepatitis C: results from the Hepatitis C Antiviral Long-term Treatment Against Cirrhosis Trial.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.14256977.15768111 ◽

2012 ◽

Author(s):

Antonio Craxi ◽

Vincenza Calvaruso

Keyword(s):

Chronic Hepatitis ◽

Hepatitis C ◽

Liver Function ◽

Clinical Outcomes ◽

Chronic Hepatitis C ◽

Liver Function Tests ◽

Term Treatment ◽

Function Tests ◽

Long Term Treatment

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Liver Impairment and Hematological Changes in Patients with Chronic Hepatitis C and COVID-19: A Retrospective Study after One Year of Pandemic

Medicina ◽

10.3390/medicina57060597 ◽

2021 ◽

Vol 57 (6) ◽

pp. 597

Author(s):

Bianca Cerbu ◽

Stelian Pantea ◽

Felix Bratosin ◽

Iulia Vidican ◽

Mirela Turaiche ◽

...

Keyword(s):

Chronic Hepatitis ◽

Hepatitis C ◽

Clinical Outcomes ◽

Chronic Hepatitis C ◽

Hcv Infection ◽

Multivariate Logistic Regression Model ◽

P Value ◽

Liver Impairment ◽

All Cause Mortality ◽

Chronic Hcv

Background and Objectives: The COVID-19 pandemic is an ongoing public health emergency. Patients with chronic diseases are at greater risk for complications and poor outcomes. The objective of this study was to investigate the liver function abnormalities and clinical outcomes in patients with COVID-19 and chronic hepatitis C. Materials and Methods: This retrospective, single-center study was conducted on a cohort of 126 patients with a history of hepatitis C, confirmed with COVID-19 between 01 April 2020 and 30 December 2020. Several clinical outcomes were compared between patients with active and non-active HCV infection, and the risks of liver impairment and all-cause mortality in active HCV patients were analyzed using a multivariate logistic regression model. Results: Among 1057 patients under follow-up for chronic HCV infection, 126 (11.9%) were confirmed with COVID-19; of these, 95 (75.4%) were under treatment or achieved SVR, while in the other 31 (24.6%), we found active HCV replication. There was a significantly higher proportion of severe COVID-19 cases in the active HCV group as compared to the non-active HCV group (32.2 vs. 7.3%, p < 0.001). Multivariate analysis showed that age, sex, alanine aminotransferase, C-reactive protein, procalcitonin, and HCV viral load were significant independent risk factors for liver impairment and all-cause mortality. The length of stay in hospital and intensive care unit for COVID-19 was significantly higher in patients with active HCV infection (p-value < 0.001), and a higher proportion of these patients required mechanical ventilation. Conclusions: Active HCV infection is an independent risk factor for all-cause mortality in COVID-19 patients.

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Intrahepatic TLR3 and IFNL3 Expressions Are Associated with Stages of Fibrosis in Chronic Hepatitis C

Viruses ◽

10.3390/v13061103 ◽

2021 ◽

Vol 13 (6) ◽

pp. 1103

Author(s):

Keyla Santos Guedes de Sá ◽

Ednelza da Silva Graça Amoras ◽

Simone Regina Souza da Silva Conde ◽

Maria Alice Freitas Queiroz ◽

Izaura Maria Vieira Cayres-Vallinoto ◽

...

Keyword(s):

Immune Response ◽

Chronic Hepatitis ◽

Viral Load ◽

Hepatitis C ◽

Chronic Hepatitis C ◽

Control Group ◽

Gene Expressions ◽

Healthy Control ◽

Advanced Stages ◽

Chronic Hcv

An inefficient immune response against the hepatitis C virus (HCV), combined with viral evasion mechanisms, is responsible for the chronicity of infection. The need to evaluate the innate mechanisms of the immune response, such as TLR3 and IFN-λ3, and their relationship with the virus–host interaction is important for understanding the pathogenesis of chronic hepatitis C. The present study aimed to investigate the gene expressions of TRL3 and IFNL3 in liver tissue, seeking to evaluate whether these could be potential biomarkers of HCV infection. A total of 23 liver biopsy samples were collected from patients with chronic HCV, and 8 biopsies were collected from healthy control patients. RNA extraction, reverse transcription and qPCR were performed to quantify the relative gene expressions of TLR3 and IFNL3. Data on the viral load; AST, ALT, GGT and AFP levels; and the viral genotype were collected from the patients′ medical records. The intrahepatic expression of TLR3 (p = 0.0326) was higher in chronic HCV carriers than in the control group, and the expression of IFNL3 (p = 0.0037) was lower in chronic HCV carriers than in the healthy control group. The expression levels of TLR3 (p = 0.0030) and IFNL3 (p = 0.0036) were higher in the early stages of fibrosis and of necroinflammatory activity in the liver; in contrast, TLR3 and IFNL3 expressions were lower in the more advanced stages of fibrosis and inflammation. There was no correlation between the gene expression and the serum viral load. Regarding the initial METAVIR scale scores, liver transaminase levels were lower in patients with advanced fibrosis when correlated with TLR3 and IFNL3 gene expressions. The results suggest that in the early stages of the development of hepatic fibrosis, TLR3 and IFN-λ3 play important roles in the antiviral response and in the modulation of the tolerogenic liver environment because there is a decrease in the intrahepatic expressions of TLR3 and IFNL3 in the advanced stages of fibrosis, probably due to viral evasion mechanisms.

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Serum Inter-Alpha-Trypsin Inhibitor Heavy Chain 4 (ITIH4) in Children with Chronic Hepatitis C: Relation to Liver Fibrosis and Viremia

Hepatitis Research and Treatment ◽

10.1155/2014/307942 ◽

2014 ◽

Vol 2014 ◽

pp. 1-7 ◽

Cited By ~ 6

Author(s):

Mostafa M. Sira ◽

Behairy E. Behairy ◽

Azza M. Abd-Elaziz ◽

Sameh A. Abd Elnaby ◽

Ehab E. Eltahan

Keyword(s):

Chronic Hepatitis ◽

Hepatitis C ◽

Liver Fibrosis ◽

Chronic Hepatitis C ◽

Heavy Chain ◽

Trypsin Inhibitor ◽

Clinical Laboratory ◽

Treatment Naïve ◽

Liver Fibrogenesis ◽

Chronic Hcv

Liver fibrosis and viremia are determinant factors for the treatment policy and its outcome in chronic hepatitis C virus (HCV) infection. We aimed to investigate serum level of inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) and its relation to liver fibrosis and viremia in children with chronic HCV. ITIH4 was measured by ELISA in 33 treatment-naive children with proved chronic HCV and compared according to different clinical, laboratory and histopathological parameters. Liver histopathological changes were assessed using Ishak score and compared with aspartate transaminase-to-platelet ratio (APRI) and FIB-4 indices as simple noninvasive markers of fibrosis. ITIH4 was measured in a group of 30 age- and sex-matched healthy controls. ITIH4 was significantly higher in patients than in controls (54.2±30.78 pg/mL versus 37.21±5.39 pg/mL; P=0.021). ITIH4, but not APRI or FIB-4, had a significant direct correlation with fibrosis stage (P=0.015, 0.961, and 0.389, resp.), whereas, the negative correlation of ITIH4 with HCV viremia was of marginal significance (P=0.071). In conclusion, ITIH4 significantly correlated with higher stages of fibrosis indicating a possible relation to liver fibrogenesis. The trend of higher ITIH4 with lower viremia points out a potential antiviral properties and further studies in this regard are worthwhile.

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Circulating and inducible IL-32α in chronic hepatitis C virus infection

Canadian Liver Journal ◽

10.3138/canlivj.2018-0003 ◽

2019 ◽

Vol 2 (1) ◽

pp. 23-30

Author(s):

Mark Collister ◽

Julia Rempel ◽

Jiaqi Yang ◽

Kelly Kaita ◽

Zach Raizman ◽

...

Keyword(s):

Chronic Hepatitis ◽

Hepatitis C Virus ◽

Hepatitis C ◽

Chronic Hepatitis C ◽

Mononuclear Cells ◽

Peripheral Blood Mononuclear ◽

Chronic Hepatitis C Virus ◽

Chronic Hcv

Background: Interleukin 32 (IL-32) is a recently described pro-inflammatory cytokine implicated in chronic hepatitis C virus (HCV)-related inflammation and fibrosis. IL-32α is the most abundant IL-32 isoform. Methods: Circulating IL-32α levels were documented in patients with chronic HCV infections ( n = 31) and compared with individuals who spontaneously resolved HCV infection ( n = 14) and HCV-naive controls ( n = 20). In addition, peripheral blood mononuclear cells (PBMC) from the chronic HCV ( n = 12) and HCV-naive ( n = 9) cohorts were investigated for responses to HCV core and non-structural (NS)3 protein induced IL-32α production. Finally, correlations between IL-32α levels, hepatic fibrosis and subsequent responses to interferon-based therapy were documented in patients with chronic HCV. Results: Circulating IL-32α levels in patients with chronic HCV were similar to those of spontaneously resolved and HCV-naive controls. HCV protein induced IL-32α responses were similar in chronic HCV patients and HCV-naive controls. In patients with chronic HCV, serum IL-32α levels correlated with worsening METAVIR fibrosis (F) scores from F0 to F3 ( r = 0.596, P < 0.001) as did NS3 induced IL-32α responses ( r = 0.837, P < 0.05). However, these correlations were not sustained with the inclusion of IL-32α levels at F4 scores, suggesting events at F4 interfere with IL-32α synthesis or release. In chronic HCV patients who underwent treatment ( n = 28), baseline in vivo and in vitro induced IL-32α concentrations were not predictive of therapeutic outcomes. Conclusions: IL-32α activity is associated with worsening fibrosis scores in non-cirrhotic, chronic HCV patients.

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Polymorphism in interferon λ3/interleukin-28B gene and risk to noncirrhotic chronic hepatitis C genotype 3 virus infection and its effect on the response to combined daclatasvir and sofosbuvir therapy

Journal of Medical Virology ◽

10.1002/jmv.25359 ◽

2018 ◽

Vol 91 (4) ◽

pp. 659-667 ◽

Cited By ~ 2

Author(s):

Anwar Jamal Khan ◽

Vivek Aanand Saraswat ◽

Prabhat Ranjan ◽

Devendra Parmar ◽

Tajwar Singh Negi ◽

...

Keyword(s):

Chronic Hepatitis ◽

Hepatitis C ◽

Virus Infection ◽

Chronic Hepatitis C ◽

Genotype 3 ◽

Interleukin 28B

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The Association of XRCC1 Gene Polymorphisms and Chronic Hepatitis C Induced Insulin Resistance in Egyptian Patients

Cells ◽

10.3390/cells7110185 ◽

2018 ◽

Vol 7 (11) ◽

pp. 185

Author(s):

Salwa Abo El-khair ◽

Mona Arafa ◽

Tarek Besheer ◽

Ahmed El-Eraky ◽

Ayman Elsamanoudy

Keyword(s):

Insulin Resistance ◽

Chronic Hepatitis ◽

Hepatitis C ◽

Chronic Hepatitis C ◽

Gene Polymorphisms ◽

Nucleotide Polymorphisms ◽

Xrcc1 Gene ◽

Egyptian Patients ◽

Pcr Rflp ◽

Chronic Hcv

Chronic hepatitis C is implicated in insulin resistance (IR) susceptibility. An X-ray repair cross-complementing group 1 gene (XRCC1) is proposed to be a candidate gene for a study of IR susceptibility. So, this study aims to investigate the possible association of the XRCC1 gene polymorphisms with the risk of IR related to chronic hepatitis C virus (HCV) infection in Egyptian patients. In a case-control study, a total of 210 subjects, including 140 chronic HCV patients (87 patients with IR and 53 without IR) and 70 healthy controls, were included. Two genetic polymorphisms (c.1254C > T and c.1517G > C) of the XRCC1 gene were genotyped via the PCR-restriction fragment length polymorphism (PCR-RFLP) technique. The result of the current study revealed that these two single nucleotide polymorphisms (SNPs) have statistically significant influences on susceptibility to IR in chronic HCV infected Egyptian patients. It could be concluded that c.1254C > T, the TT genotype, CT/CC carriers as well as c.1517G > C, the CC genotype and GC/GG carriers might be associated with increased IR susceptibility. Moreover, T-allele of c.1254C > T and the C-allele of c.1517G > C genetic variants might influence the susceptibility.

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