scholarly journals Elevated serum levels of adiponectin and interlukin-28B after IFN/RIB therapy in hepatitis C virus-infected patients

2019 ◽  
Vol 13 (05) ◽  
pp. 434-444
Author(s):  
Kaveh Sadeghi ◽  
Abbas Ahmadi Vasmehjani ◽  
Rasoul Baharlou ◽  
Zamaneh Hajikhezri ◽  
Seyed Jalal Kiani
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Elevated Serum ◽  
Serum Levels ◽  
Clinicopathological Parameters ◽  
Il28b Genotype ◽  
Adiponectin Receptors ◽  
Specific Primers ◽  
Interleukin 28B ◽  
Genotype 3A

Introduction: The interleukin 28B (IL28B) genotype is associated with changes of lipid metabolism in patients infected with hepatitis C virus (HCV). The association of steatosis with serum levels of adiponectin in chronic hepatitis C (CHC) patients has also been documented. This study aimed for the evaluation of serum levels of IL28B and adiponectin as well as the association of IL28B SNPs with different clinicopathological parameters in HCV-infected patients. Methodology: All 142 HCV-infected patients received peg-interferon plus ribavirin. Detection of rs8099917 and rs12979860 IL-28B genotypes was done with specific primers. Serum IL28 and adiponectin levels were measured using commercial ELISA kits. Results: Higher levels of both IL28 and adiponectin were found in patients. In Genotype 3a (G3a) -infected patients, IL28 and adiponectin serum levels were significantly higher than those infected with G1a. A correlation was found between increasing levels of AST and ALT in G3a-infected patients and the decrease in IL28 and adiponectin serum levels, respectively, in contrast to G1a-infected patients. Higher levels of both IL28 and adiponectin were associated with both CT allele of rs12979860 and TT allele of rs8099917 in patients in comparison with corresponding alleles in controls. Conclusions: In contrast to other studies, this study showed higher serum adiponectin levels in HCV-infected patients compared to that in healthy controls. This finding is possibly due to adiponectin resistance caused by down-regulation of adiponectin receptors or tumorigenic effects of adiponectin. Our genotype-based analyses revealed, at least in part, the involvement of the viral factors in the outcome of HCV infection.

scholarly journals Elevated Serum Levels of Interferon‐γ–Inducible Protein–10 in Patients Coinfected with Hepatitis C Virus and HIV

2007 ◽  
Vol 196 (7) ◽  
pp. 1053-1057 ◽  
Author(s):  
Barbara Roe ◽  
Suzie Coughlan ◽  
Jaythoon Hassan ◽  
Anne Grogan ◽  
Gillian Farrell ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Elevated Serum ◽  
Serum Levels ◽  
Interferon Γ ◽  
Inducible Protein

Associations between responses to interferon therapy and genetic variation in interleukin-28B and the core region of hepatitis C virus genotype 3a

2015 ◽  
Vol 87 (8) ◽  
pp. 1361-1367
Author(s):  
Keiichi Yamada ◽  
Masatoshi Ishigami ◽  
Teiji Kuzuya ◽  
Takashi Honda ◽  
Kazuhiko Hayashi ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Interferon Therapy ◽  
Core Region ◽  
Virus Genotype ◽  
The Core ◽  
Interleukin 28B ◽  
Genotype 3A

Association of Interleukin 28B Polymorphism with Clearance of Hepatitis C Virus: A Mini Review

2020 ◽  
Vol 30 (3) ◽  
pp. 223-229
Author(s):  
Mahrukh Shaheen ◽  
Samia Afzal ◽  
Bushra Khubaib ◽  
Iram Amin ◽  
Muhammad Shahid ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Interleukin 28B

The hepatitis C virus NS5A protein and response to interferon α: mutational analyses in patients with chronic HCV genotype 3a infection from India

2006 ◽  
Vol 196 (1) ◽  
pp. 11-21 ◽  
Author(s):  
Ankur Goyal ◽  
Wolf P. Hofmann ◽  
Eva Hermann ◽  
Stella Traver ◽  
Syed S. Hissar ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Interferon Α ◽  
Hcv Genotype ◽  
Ns5a Protein ◽  
Chronic Hcv ◽  
Genotype 3A

Oncogenic transcriptomic profile is sustained in the liver after the eradication of the hepatitis C virus

2021 ◽  
Author(s):  
Haruhiko Takeda ◽  
Atsushi Takai ◽  
Eriko Iguchi ◽  
Masako Mishima ◽  
Soichi Arasawa ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Molecular Basis ◽  
Elevated Serum ◽  
Gene Clusters ◽  
Viral Clearance ◽  
Hcv Infection ◽  
Transcriptomic Profile ◽  
Direct Acting ◽  
Liver Tissues

Abstract Hepatocellular carcinoma (HCC) developing after hepatitis C virus (HCV) eradication is a serious clinical concern. However, molecular basis for the hepatocarcinogenesis after sustained virologic response (SVR) remains unclear. In this study, we aimed to unveil the transcriptomic profile of post-SVR liver tissues and explore the molecules associated with post-SVR carcinogenesis. We analysed 90 RNA-sequencing datasets, consisting of noncancerous liver tissues including 20 post-SVR, 40 HCV-positive and 7 normal livers, along with Huh7 cell line specimens before and after HCV infection and eradication. Comparative analysis demonstrated that cell cycle- and mitochondrial function-associated pathways were altered only in HCV-positive noncancerous liver tissues, while some cancer-related pathways were upregulated in the noncancerous liver tissues of both post-SVR and HCV-positive cases. The persistent upregulation of carcinogenesis-associated gene clusters after viral clearance was reconfirmed through in vitro experiments, of which, CYR61, associated with liver fibrosis and carcinogenesis in several cancer types, was the top enriched gene and co-expressed with cell proliferation-associated gene modules. To evaluate whether this molecule could be a predictor of hepatocarcinogenesis after cure of HCV infection, we also examined 127 sera from independent HCV-positive cohorts treated with direct-acting antivirals, including 60 post-SVR-HCC patients, and found that the elevated serum Cyr61 was significantly associated with early carcinogenesis after receiving direct-acting antiviral therapy. In conclusion, some oncogenic transcriptomic profiles are sustained in liver tissues after HCV eradication, which might be a molecular basis for the liver cancer development even after viral clearance. Among them, upregulated CYR61 could be a possible biomarker for post-SVR HCC.

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