Progress on influencing factors and biomarkers for hepatic fibrosis progression of hepatitis C

doi:10.3877/cma.j.issn.1674-1358.2024.01.001

Abstract

Abstract:

Hepatitis C is a common infectious disease caused by hepatitis C virus (HCV) infection. According to the World Health Organization, there are approximately 58 million cases of chronic hepatitis C worldwide, with about 1.5 million new infected cases each year. While direct-acting antiviral agents can make hepatitis C a curable disease, which often progresses silently, and some patients discover the disease when it has already advanced to the stage of liver fibrosis, or even liver cirrhosis and liver cancer. Early-stage liver fibrosis can be reversed with medication, but in some patients, fibrosis can still progress despite achieving sustained biochemical and virological responses to drug treatment, leading to a poor prognosis. Therefore, it is crucial to study the factors that influence the progression of the liver cirrhosis of patients with hepatitis C. Early diagnosis, intervention and treatment of liver fibrosis caused by hepatitis C are all important aspects of clinical practice. However, currently available indicators for diagnosing liver fibrosis have certain limitations. Serological markers are not sensitive enough for early diagnosis of liver fibrosis in hepatitis C, thus there is an urgent need for new biological markers to assist in clinical diagnosis and enable early intervention and treatment of liver fibrosis. This article summarizes the main influencing factors of liver fibrosis in hepatitis C progression from three aspects: host, pathogen and external factors. It also elucidates the research progress of biomarkers associated with the staging of liver fibrosis in hepatitis C, providing reference for early diagnosis, intervention and delayed progression of liver fibrosis caused by hepatitis C.

Key words: Hepatitis C, Liver fibrosis, Influencing factor, Biomarker

Qi Zhang, Zhen Ma. Progress on influencing factors and biomarkers for hepatic fibrosis progression of hepatitis C[J]. Chinese Journal of Experimental and Clinical Infectious Diseases(Electronic Edition), 2024, 18(01): 1-6.

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References 49

[1]	World Health Organization. Global progress report on HIV, viral hepatitis and se-xually transmitted infections, 2021[EB/OL]. (2021-07-15) [2023-01-20]. URL
[2]	Missiha SB, Ostrowski M, Heathcote EJ. Disease progression in chronic hepatitis C: modifiable and nonmodifiable factors[J]. Gastroenterology,2008,134(6):1699-1714.
[3]	Bouayad A, Laamiri FZ, Elmoumou L, et al. Prevalence of liver fibrosis and cirrhosis in 699 Moroccan patients with chronic hepatitis C[J]. Pan Afr Med J,2021,12(39):32.
[4]	陈晓倩. 东北某地区丙型肝炎病毒感染者疾病转归调查及影响肝纤维化进展的因素分析[D]. 长春市:吉林大学,2019.
[5]	Bakr I, Rekacewicz C, El Hosseiny M, et al. Higher clearance of hepatitis C virus infection in females compared with males[J]. Gut,2006,55(8):1183-1187.
[6]	孔菲. 丙型肝炎病毒自发清除及肝纤维化进展的影响因素[D]. 长春市: 吉林大学,2014.
[7]	Shchanitcyna SE, Burnevich EZ, Nikulkina EN, et al. Risk factors of unfavorable prognosis of chronic hepatitis C[J]. Ter Arkh,2019,91(2):59-66.
[8]	Nickbakhsh S, McWilliam Leitch EC, Smith S, et al. Geographical variation in hepatitis C-related severe liver disease and patient risk factors: a multicentre cross-sectional study[J]. Epidemiol Infect,2023,151:e59.
[9]	Ruggieri A, Gagliardi MC, Anticoli S. Sex-dependent outcome of hepatitis B and C viruses infections: synergy of sex hormones and immune responses?[J]. Front Immunol,2018,9:2302.
[10]	Tanwar S, Rhodes F, Srivastava A, et al. Inflammation and fibrosis in chronic liver diseases including non-alcoholic fatty liver disease and hepatitis C[J]. World J Gastroenterol,2020,26(2):109-133.
[11]	Đorđević V, Stanković Đorđević D, Kocić B, et al. The impact of hepatitis C virus genotypes on oxidative stress markers and catalase activity[J]. Oxid Med Cell Longev,2021,2021:6676057.
[12]	Ciardullo S, Mantovani A, Ciaccio A, et al. Hepatitis C virus infection and diabetes: A complex bidirectional relationship[J]. Diabetes Res Clin Pract,2022,187:109870.
[13]	Ding Y, Li G, Zhou Z, et al. Molecular mechanisms underlying hepatitis C virus infection-related diabetes[J]. Metabolism,2021,121: 154802.
[14]	朱桂晓, 边城. 慢性丙型肝炎发展至肝硬化的临床危险因素分析[J]. 中国社区医师,2015,31(11):44-45.
[15]	周奕, 苏明华, 江建宁, 等. 慢性丙型肝炎患者不同感染途径的临床特点分析及自然病程[J]. 实用医学杂志,2018,34(11):1791-1794, 1799.
[16]	Li W, Liang J, An J, et al. Geographic distribution of HCV genotypes and efficacy of direct-acting antivirals in chronic HCV-infected patients in North and Northeast China: A real-world multicenter study[J]. Can J Gastroenterol Hepatol,2022,2022:7395506.
[17]	Parczewski M, Kordek J, Janczewska E, et al. Hepatitis C virus (HCV) genotype 1 NS5A resistance-associated variants are associated with advanced liver fibrosis independently of HCV-transmission clusters[J]. Clin Microbiol Infect,2019,25(4):513.
[18]	Chen X, Liu X, Duan S, et al. Plasma inflammatory biomarkers associated with advanced liver fibrosis in HIV-HCV-coinfected individuals[J]. Int J Environ Res Public Health,2020,17(24):9474.
[19]	Monnig MA, Cohen R, Ramratnam B, et al. HIV infection, HCV coinfection, and alcohol use: associations with microbial translocation and immune activation[J]. Alcohol Clin Exp Res,2019,43(6):1126-1134.
[20]	de Brito WB, Queiroz MAF, da Silva Graça Amoras E, et al. The TGFB1-509C/T polymorphism and elevated TGF-β1 levels are associated with chronic hepatitis C and cirrhosis[J]. Immunobiology, 2020,225(5):152002.
[21]	Li W, Duan X, Zhu C, et al. Hepatitis B and hepatitis C virus infection promote liver fibrogenesis through a TGF-β1-induced OCT4/Nanog pathway[J]. J Immunol,2022,208(3):672-684.
[22]	Seronello S, Montanez J, Presleigh K, et al. Ethanol and reactive species increase basal sequence heterogeneity of hepatitis C virus and produce variants with reduced susceptibility to antivirals[J]. PLoS One,2011,6(11):e27436.
[23]	Xu HQ, Wang CG, Zhou Q, et al. Effects of alcohol consumption on viral hepatitis B and C[J]. World J Clin Cases,2021,9(33):10052- 10063.
[24]	Martín-González C, Pelazas-González R, Fernández-Rodríguez C, et al. Ferritin and liver fibrosis among patients with chronic hepatitis C virus infection[J]. J Trace Elem Med Biol,2020,61:126542.
[25]	Shirabe K, Bekki Y, Gantumur D, et al. Mac-2 binding protein glycan isomer (M2BPGi) is a new serum biomarker for assessing liver fibrosis: more than a biomarker of liver fibrosis[J]. J Gastroenterol, 2018,53(7):819-826.
[26]	Mermutluoğlu Ç, Tekin R, Tekin RC, et al. Evulation of prolidase enzyme, and galectin levels as a marker for fibrosis in patients with chronic hepatitis B[J]. Eur Rev Med Pharmacol Sci,2022,26(24):9467-9472.
[27]	Gruszewska E, Grytczuk A, Chrostek L. Glycosylation in viral hepatitis[J]. Biochim Biophys Acta Gen Subj,2021,1865(11):129997.
[28]	Kurtenkov O, Jakovleva J, Sergejev B, et al. Association of the sialylation of antibodies specific to the HCV E2 envelope glycoprotein with hepatic fibrosis progression and antiviral therapy efficacy[J]. Dis Markers,2020,2020:8881279.
[29]	Batsaikhan B, Lu MY, Yeh ML, et al. Elevated interleukin-4 levels predicted advanced fibrosis in chronic hepatitis C[J]. J Chin Med Assoc,2019,82(4):277-281.
[30]	Aoudjehane L, Podevin P, Scatton O, et al. Interleukin-4 induces human hepatocyte apoptosis through a Fas-independent pathway[J]. FASEB J,2007,21(7):1433-44.
[31]	Stanley TL, Fourman LT, Zheng I, et al. Relationship of IGF-1 and IGF-binding proteins to disease severity and glycemia in nonalcoholic fatty liver disease[J]. J Clin Endocrinol Metab,2021,106(2):e520-e533.
[32]	Saeki C, Kanai T, Ueda K, et al. Insulin-like growth factor 1 predicts decompensation and long-term prognosis in patients with compensated cirrhosis[J]. Front Med (Lausanne),2023,24(10):1233928.
[33]	Fraenkel E, Lazurova I. IGF-1 and IGFBP3 as indirect markers of hepatic insulin resistance and their relation to metabolic syndrome parameters in liver steatosis patients[J]. Endocr Regul,2023,57(1):69- 79.
[34]	Colak Y, Senates E, Ozturk O, et al. Serum concentrations of human insulin-like growth factor-1 and levels of insulin-like growth factor-binding protein-5 in patients with nonalcoholic fatty liver disease: association with liver histology[J]. Eur J Gastroenterol Hepatol, 2012,24(3):255-261.
[35]	Cao LH, Lu FM, Lu XJ, et al. Study on the relationship between insulin growth factor 1 and liver fibrosis in patients with chronic hepatitis C with type 2 diabetes mellitus[J]. J Cell Biochem, 2018,119(11):9513-9518.
[36]	Helaly GF, Hussein NG, Refai W, et al. Relation of serum insulin-like growth factor-1 (IGF-1) levels with hepatitis C virus infection and insulin resistance[J]. Transl Res,2011,158(3):155-162.
[37]	Yang XJ, Wang XO, Chen Y, et al. Associations of content and gene polymorphism of macrophage inhibitory factor-1 and chronic hepatitis C virus infection[J]. World J Gastroenterol,2020,26(41):6378-6390.
[38]	Ye S, Chen Y, Lou X, et al. Association of macrophage inhibitory factor-1 polymorphisms with antiviral efficacy of type 1b chronic hepatitis C[J]. Mol Cell Biochem,2021,476(6):2439-2447.
[39]	Myojin Y, Hikita H, Sugiyama M, et al. Hepatic stellate cells in hepatocellular carcinoma promote tumor growth via growth differentiation factor 15 production[J]. Gastroenterology,2021, 160(5):1741-1754. e16.
[40]	Qi P, Ma MZ, Kuai JH. Identification of growth differentiation factor 15 as a pro-fibrotic factor in mouse liver fibrosis progression[J]. Int J Exp Pathol,2021,102(3):148-156.
[41]	王莉. 血管内皮生长因子和损伤标志物在丙型病毒性肝炎感染肝纤维化患者中的表达及其临床意义[J]. 山西医药杂志,2022,51(7):757-760.
[42]	李思佳, 孙小蒙. 血管内皮生长因子与糖尿病肾病关系的研究进展[J]. 医学综述,2019,25(3):515-519.
[43]	Hu K, Babapoor-Farrokhran S, Rodrigues M, et al. Correction: Hypoxia-inducible factor 1 upregulation of both VEGF and ANGPTL4 is required to promote the angiogenic phenotype in uveal melanoma[J]. Oncotarget,2021,12(5):519-520.
[44]	Ma JC, Huang X, Shen YW, et al. Tenascin-C promotes migration of hepatic stellate cells and production of type Ⅰ collagen[J]. Biosci Biotechnol Biochem,2016,80(8):1470-1477.
[45]	Bhattacharyya S, Midwood KS, Varga J. Tenascin-C in fibrosis in multiple organs: Translational implications[J]. Semin Cell Dev Biol,2022,128(1084-9521):130-136.
[46]	李彦英, 黄平, 张治, 等. 宫颈癌患者血清S100A14和LOXL2的表达水平及临床意义[J]. 国际检验医学杂志,2023,44(1):40-43, 48.
[47]	Vadasz Z, Kessler O, Akiri G,et al. Abnormal deposition of collagen around hepatocytes in Wilson’s disease is associated with hepatocyte specific expression of lysyl oxidase and lysyl oxidase like protein-2[J]. J Hepatol,2005,43(3):499-507.
[48]	Altinbas A, Holmes JA, Salloum S, et al. LOXL-2 and TNC-C are markers of liver fibrogenesis in HCV/HIV-, HIV- and HCV-infected patients[J]. Biomark Med,2022,16(11):839-846.
[49]	Rosenbloom J, Ren S, Macarak E. New frontiers in fibrotic disease therapies: The focus of the Joan and Joel Rosenbloom Center for Fibrotic Diseases at Thomas Jefferson University[J]. Matrix Biol,2016,51(0945-053X):14-25.

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