Immunophysiological Effects of of Hepatitis B Virus Genotypic Variations on Interleukin-35 Levels
Article Sidebar
Page Numbers:
562-569
Digital Object Identifier:
10.58578/ajstea.v4i4.10046
Viewed: 0 times
Downloaded: 0 times
LYAS Publisher cordially invites qualified professionals to serve as Editors or Reviewers. Your expertise will make an important contribution to maintaining and strengthening the academic quality of our publications. Interested applicants are kindly requested to complete the application form at the following link: Editors & Reviewers
Please feel free to contact us if you need any further information about the submission process or if you have any additional questions.
Authors:Ahmed Talib Yassen Aldossary1*
Copyright :Authors retain copyright and grant the journal right of first publication.
Main Article Content
Abstract
Hepatitis B virus (HBV) remains a major global health concern, with viral genetic diversity playing an important role in immune evasion and disease persistence. Interleukin-35 (IL-35) is a potent immunosuppressive cytokine that may facilitate HBV persistence; however, its relationship with HBV genotypic variation remains insufficiently understood. This study investigated the association between HBV genotypes and serum IL-35 concentrations among patients with HBV infection. A total of 150 participants were enrolled, comprising 60 patients with chronic hepatitis B (CHB), 60 inactive HBV carriers, and 30 healthy controls. HBV genotypes were identified using polymerase chain reaction-based methods, while serum IL-35 concentrations were quantified using an enzyme-linked immunosorbent assay. Serum IL-35 concentrations were significantly higher among patients with CHB (85.4 ± 12.3 pg/mL) than among healthy controls (p < 0.001). Patients infected with HBV genotype C also exhibited significantly higher IL-35 concentrations than those infected with genotype D (p = 0.021). Furthermore, serum IL-35 concentrations were strongly and positively correlated with HBV DNA viral load. These findings indicate that HBV genotype C is associated with a stronger IL-35-mediated immunosuppressive response, which may contribute to viral chronicity and more severe clinical outcomes. This study provides evidence of genotype-specific immune modulation in HBV infection and highlights the potential relevance of IL-35 in evaluating viral persistence and disease progression.
Citation Metrics:
Downloads
Citation Metrics & Similar Scopus Articles
-
Liu Q. (2027)Elucidating the Respective Roles of Photochemical and Photothermal Effects in Photocatalytic Methanol DecompositionNano Micro Letters, 19(1)
-
Berenjian K. (2027)Impact of Mild Traumatic Brain Injury (mTBI) on CYP2D6 Activity and the Restorative Effects of Melatonin and Vitamin C SupplementationIranian Journal of Pharmaceutical Research, 26(1)
-
Sheng T. (2027)Photothermal Superhydrophobic Textiles: An Emerging Paradigm from Passive Water Repellency to Active Thermal ManagementNano Micro Letters, 19(1)
Article Details
Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
References
World Health Organization. (2026, July 28). Hepatitis B. https://www.who.int/news-room/fact-sheets/detail/hepatitis-b
Velkov, S., Ott, J. J., Protzer, U., & Michler, T. (2018). The global hepatitis B virus genotype distribution approximated from available genotyping data. Genes, 9(10), 495. https://doi.org/10.3390/genes9100495
Fernandes da Silva, C., Keeshan, A., & Cooper, C. (2023). Hepatitis B virus genotypes influence clinical outcomes: A review. Canadian Liver Journal, 6(3), 347–352. https://doi.org/10.3138/canlivj-2023-0003
Li, X., Liu, X., & Wang, W. (2021). IL-35: A novel immunomodulator in hepatitis B virus-related liver diseases. Frontiers in Cell and Developmental Biology, 9, 614847. https://doi.org/10.3389/fcell.2021.614847
Xiang, X. G., & Xie, Q. (2015). IL-35: A potential therapeutic target for controlling hepatitis B virus infection. Journal of Digestive Diseases, 16(1), 1–6. https://doi.org/10.1111/1751-2980.12218
Al-Azzawi, R. H., Mohsen, R. T., & Ad’hiah, A. H. (2020). Serum level of interleukin-35 in patients with chronic hepatitis B virus infection. Iraqi Journal of Science, 61(11), 2860–2865. https://doi.org/10.24996/ijs.2020.61.11.9
Lin, C. L., & Kao, J. H. (2015). Hepatitis B virus genotypes and variants. Cold Spring Harbor Perspectives in Medicine, 5(5), a021436. https://doi.org/10.1101/cshperspect.a021436
Li, Y., Geng, J., Geng, J., & Wei, L. (2023). The role of interleukin-35 in viral hepatitis. International Immunopharmacology, 115, 109675.
Thakur, V., Guptan, R. C., & Sarin, S. K. (2022). Relevance of hepatitis B virus genetic variations in disease progression and response to therapy. Journal of Clinical and Experimental Hepatology, 12(2), 541–555.
Zhang, J., Zhang, Y., & Piao, M. (2021). Interleukin-35 in the development and progression of liver diseases. Mediators of Inflammation, 2021, 6654702.
European Association for the Study of the Liver. (2017). EASL 2017 clinical practice guidelines on the management of hepatitis B virus infection. Journal of Hepatology, 67(2), 370–398. https://doi.org/10.1016/j.jhep.2017.03.021
Huang, A., Lan, T., & Peng, J. (2023). IL-35 in chronic hepatitis B: A double-edged sword for immune regulation. Journal of Viral Hepatitis, 30(5), 412–422.
Wang, L., Meng, X., & Ju, Y. (2022). Impact of HBV genotypes on the secretion of inhibitory cytokines in chronic infection. Frontiers in Immunology, 13, 901235.
Chen, J., Liu, G., & Zhang, L. (2021). Relationship between IL-35 levels and HBV DNA viral load in patients with different genotypes. Medical Microbiology and Immunology, 210(3), 145–153.
Xiang, X., Liu, Y., & Li, Y. (2024). Interleukin-35 contributes to the progression of hepatitis B virus-related liver diseases. International Journal of Infectious Diseases, 140, 106–114.