Exploration of IL-32 (rs45499297) gene variations in EBV and MS patients

Authors

  • Aya R. Abood Department Biology, Molecular Virology, College of Science, University of Baghdad, Baghdad, Iraq
  • Hula Y. Fadhil Department Biology, Molecular Virology, College of Science, University of Baghdad, Baghdad, Iraq

DOI:

https://doi.org/10.31351/vol33iss2pp170-178

Abstract

Interleukin-32 is a multifunctional cytokine linked to a variety of illnesses and inflammatory disorders, the central nervous system is affected by the chronic inflammatory disease known as multiple sclerosis (MS). Studies about found relationship between them are rare and inconclusive specially when MS patients with Epstein-Barr virus (EBV) positive. Recently, IL-32 identified increase and considers proinflammatory following EBV infection. A case-control study (79 MS patients and 108 controls) for the purpose of investigating T/C genotype of (rs45499297) in all participant then identify their role in MS and EBV patients by Restriction fragment length polymorphism (RFLP) technique. The results appeared that alleles and genotype (rs45499297) was no significant differences between MS patients and healthy controls, also between groups of expanded disability status scale in MS patients but with EBV infection was results appeared that allele C of( rs45499297) more effector in MS patients than controls. The mean of EBV load among multiple sclerosis patients according to sex, EDSS, and therapy line the results revealed that elevated viral load in male, EDSS ≥ 3.0 and in second line therapy compare to opposite groups. In conclusion, the study indicated the role of sex and MS activity in susceptibility to EBV reactivation. However, analysis of the IL-32 gene variants (rs45499297) may influence susceptibility to EBV along with MS associated with the allele C occurrence.

 

 

References

Compston, A., H. Winedl, and B. Kieseier, Coles. Multiple sclerosis. Lancet, 2008.4(4) 372: p. 1502-1517.

Walton, C., et al., Rising prevalence of multiple sclerosis worldwide: Insights from the Atlas of MS. Multiple Sclerosis Journal, 2020. 26(14): p.1821-1816.

Weiner, H.L., A shift from adaptive to innate immunity: a potential mechanism ofdisease progression in multiple sclerosis. Journal of neurology, 2008. 255: p. 3-11.

Hatch, M.N., et al., Endogenous remyelination is induced by transplant rejectionin a viral model of multiple sclerosis. Journal of neuroimmunology, 2009. 212(1-2): p. 74-81.

Bar-Or, A., et al., Epstein–Barr virus in multiple sclerosis: theory and emerging immunotherapies. Trends in molecular medicine, 2020. 26(3): p. 296.310-

Toussirot, É. and J. Roudier, Epstein–Barr virus in autoimmune diseases. Bestpractice & research Clinical rheumatology, 2008. 22(5): p. 883-896.

Ressing, M.E., et al., Immune evasion by Epstein-Barr virus. Epstein Barr VirusVolume 2: One Herpes Virus: Many Diseases, 2015.391: p. 355-381.

Hong, J.T., et al., Interleukin 32, inflammation and cancer. Pharmacology & therapeutics, 2017. 174: p. 127-137.

Chomczynski, P. and N. Sacchi, The single-step method of RNA isolation by acid guanidinium thiocyanate–phenol–chloroform extraction: twenty-something years on. Nature protocols, 2006. 1(2): p. 581-585.

Netea, M.G., et al., IL-32 synergizes with nucleotide oligomerization domain (NOD) 1 and NOD2 ligands for IL-1β and IL-6 production through a caspase 1- dependent mechanism. Proceedings of the National Academy of Sciences, 2005.102(45): p. 16309-16314.

Meyer, N., et al., IL-32 is expressed by human primary keratinocytes and modulates keratinocyte apoptosis in atopic dermatitis. Journal of Allergy and Clinical Immunology, 2010. 125(4): p. 858-865. e10.

de Albuquerque, R., et al., The role of Interleukin‐32 in autoimmunity. Scandinavian Journal of Immunology, 2021. 93(2): p. e13012.

Kim, S.-H., et al., Interleukin-32: a cytokine and inducer of TNFα. Immunity,2005. 22(1): p. 131-142.

de Albuquerque, R., et al., The role of Interleukin‐32 in autoimmunity. Scandinavian Journal of Immunology, 2021. 93(2): p. e13012.

B.Cinar and Y. Yorgun, “What we learned from the history of multiple sclerosis measurement: expanded disability status scale”. Archives of Neuropsychiatry, 2018. 55(Suppl 1): p. S69.

Martínez Pérez, L.A., et al., Relation of serum IL-32 levels and gene polymorphism rs45499297 with obesity in Mexican patients: a laboratory and in silico analysis. 2022.

Dobson, R. and G. Giovannoni, Multiple sclerosis–a review. European journal of neurology, 2019. 26(1): p. 27-40.

Guan, Y., et al., The role of Epstein-Barr virus in multiple sclerosis: from molecular pathophysiology to in vivo imaging. Neural regeneration research, 2019. 14(3): p. 373.

Greenfield, A.L. and S.L. Hauser, B‐cell Therapy for Multiple Sclerosis: Entering an era. Annals of neurology, 2018. 83(1): p. 13-26.

Ad'hiah, A.H., N.S. Atiyah, and H.Y. Fadhil, Qualitative and Quantitative Molecular Analysis of Epstein-Barr Virus in Iraqi Patients with Relapsing- Remitting Multiple Sclerosis. Iraqi Journal of Science, 2023.64(1): p. 127-137.

Atiyah, N.S., H.Y. Fadhil, and A.H. Ad’hiah, Toll-like receptor 10 gene polymorphism and risk of multiple sclerosis among Iraqi patients. Egyptian Journal of Medical Human Genetics, 2022. 23(1): p. 88.

Aslani, S., et al., Epigenetic modifications and therapy in multiple sclerosis. Neuromolecular medicine, 2017. 19: p. 11-23.

Hollenbach, J.A. and J.R. Oksenberg, The immunogenetics of multiple sclerosis: A comprehensive review. Journal of autoimmunity, 2015. 64: p. 13-25.

Beecham, A., et al., International Multiple Sclerosis Genetics Consortium (IMSGC). Analysis of immune-related loci identifies 48 new susceptibility variants for multiple sclerosis. Nat Genet, 2013. 45(11): p. 1353-60.

Maier, L.M., et al., IL2RA genetic heterogeneity in multiple sclerosis and type 1diabetes susceptibility and soluble interleukin-2 receptor production. PLoS genetics, 2009. 1(5): p. e1000322

Hoffjan, S., et al., Association of TNFAIP 3 and TNFRSF 1 A variation with multiple sclerosis in a German case–control cohort. International journal of immunogenetics, 2015. 42(2): p. 106-110.

Martínez Pérez, L.A., et al., Relation of serum IL-32 levels and gene polymorphism rs45499297 with obesity in Mexican patients: a laboratory and in silico analysis. 2022. 39(2):313-319.

Abed Alhussien ThA, and Fadhil H.Exploring the Role of Caspase-3 and IL32 in SARS- Cov-2 Infection among Iraqi Patients. Iraqi Journal of Science,2023;64(8).

S. Rasool et al., Increased level of IL-32 during human immunodeficiency virus infection suppresses HIV replication. Immunology letters,2008.117(2):p. 161-167.

Seillet, C., et al., Estradiol promotes functional responses in inflammatory and steady-state dendritic cells through differential requirement for activation function-1 of estrogen receptor α. The Journal of Immunology, 2013. 190(11): p. 5459-5470.

Trenova, A.G., et al., Female sex hormones and cytokine secretion in women with multiple sclerosis. Neurological research, 2013. 35(1): p. 95-99.

Noyola-Martínez, N., A. Halhali, and D. Barrera, Steroid hormones and pregnancy. Gynecological Endocrinology, 2019. 35(5): p. 376-384.

Robinson, D.P. and S.L. Klein, Pregnancy and pregnancy-associated hormones alter immune responses and disease pathogenesis. Hormones and behavior, 2012. 62(3): p. 263-271.

J. R. Kerr, “Epstein-Barr virus (EBV) reactivation and therapeutic inhibitors,” Journal of Clinical Pathology, 2019. 72(10), pp. 651–658.

Lindsey, J., et al., Quantitative PCR for Epstein–Barr virus DNA and RNA in multiple sclerosis. Multiple Sclerosis Journal, 2009. 15(2): p. 153-158.

Mandal P, Gupta A, Fusi-Rubiano W, Keane PA, Yang Y. Fingolimod: therapeutic mechanisms and ocular adverse effects. Eye (Lond). 2017.31(2):232-240.

Ferreira, V.L., et al., Cytokines and interferons: types and functions. Autoantibodies and cytokines, 2018. 13.

Morsaljahan, Z., et al., Association between interleukin-32 polymorphism and multiple sclerosis. Journal of the Neurological Sciences, 2017. 379: p. 144-150.

Lai, K.-Y., et al., Maintenance of Epstein-Barr virus latent status by a novel mechanism, latent membrane protein 1-induced interleukin-32, via the protein kinase Cδ pathway. Journal of virology, 2015. 89(11): p. 5968-5980.

Downloads

Published

2024-07-03