Immunological Prevalence of EBV in Rheumatoid Arthritis Iraqi Patients

Wafaa Ayad  Al-Nuaimy; Dunya Fareed Salloom

doi:10.30526/38.3.3516

Authors

Wafaa Ayad Al-Nuaimy Department of Biology, College of Science, University of Baghdad, Baghdad, Iraq https://orcid.org/0000-0003-1066-1091
Dunya Fareed Salloom Department of Biology, College of Science, University of Baghdad, Baghdad, Iraq https://orcid.org/0000-0003-0379-1584

DOI:

https://doi.org/10.30526/38.3.3516

Keywords:

Epstein-Barr virus, viral capsid Ag, Epstein Barr nuclear Ag, Rheumatoid arthritis

Abstract

It has been hypothesized that infection with the Epstein-Barr virus (EBV) may play a role in the development of autoimmune illnesses, including rheumatoid arthritis (RA). This study aimed to investigate whether or not a history of infection with the virus is more common in RA patients compared to controls. Ninety samples ranging from 20 to 70 years old were obtained (45 patients plus 45 controls) between October 2022 and March 2023; each group included 37 females and 8 males. Rheumatoid arthritis (RA) patients who were chosen for this study were sent with a physician report for RA regular tests at Baghdad Teaching Hospital in Baghdad Province. The apparently healthy individuals were obtained (from family, friends, and other acquaintances after routine examinations) with age and sex matched with patients. We immunologically examined all 90 samples to detect Epstein-Barr virus (EBV) infection using both Epstein-Barr viral capsid Ag (VCA) IgG and Epstein Barr nuclear Ag (EBNA) IgG enzyme-linked immunosorbent assay (ELISA). The results showed that (66.7%) of RA patients and (60%) of controls were positive for VCA, while (57.8%) and (51.1%) were positive for EBNA in patients and controls, respectively. According to disease activity, there were (33.33%) and (34.62%) at high disease activity, while (66.67%) and (65.38%) at moderate disease activity were positive for VCA and EBNA, respectively. In conclusion, these findings do not reveal a relationship between EBV seroprevalence and RA, and as a result, they do not support the concept that a previous infection with EBV predisposes individuals to the development of RA

Author Biographies

Wafaa Ayad Al-Nuaimy , Department of Biology, College of Science, University of Baghdad, Baghdad, Iraq

Department of Biology, Collegeof Science, University of Baghdad, Baghdad, Iraq
Dunya Fareed Salloom, Department of Biology, College of Science, University of Baghdad, Baghdad, Iraq

Department of Biology, Collegeof Science, University of Baghdad, Baghdad, Iraq

References

1. Salloom DF, Fadhil HY, Abbas AH. Evaluation of leptin in sera of a sample of rheumatoid arthritis of Iraqi patients. Int J Recent Scient Res. 2013;4(4):004–005.

2. Guo Q, Wang Y, Xu D, Nossent J, Pavlos NJ, Xu J. Rheumatoid arthritis: pathological mechanisms and modern pharmacologic therapies. Bone Res. 2018;6:15. https://doi.org/10.1038/s41413-018-0016-9

3. Khayon LH, Farhan AA, Salloom DF. Association of interleukin 12B polymorphism and serum level of interleukin 12 in a sample of Iraqi patients with rheumatoid arthritis. Egypt J Hosp Med. 2023;90(2):2071–2073. https://doi.org/10.21608/ejhm.2023.285034

4. Ahmed DM, Salloom DF. The association between toll like receptor 7 and hepatitis C virus in a sample of Iraqi rheumatoid arthritis patients. J Global Pharma Technol. 2018;10(11 Suppl):01–08.

5. Nazar LA, Abass EA. Study of IL 33 and IL 1R4 in Iraqi rheumatoid arthritis female patients with and without dyslipidemia prone to atherosclerosis. Ibn Al Haitham J Pure Appl Sci. 2019;32(1):48–56. https://doi.org/10.30526/32.1.1920

6. Costenbader KH, Karlson EW. Epstein–Barr virus and rheumatoid arthritis: is there a link? Arthritis Res Therap. 2006;8:204. https://doi.org/10.1186/ar1893

7. Ali S, Salloom DF. A novel finding of interleukin 9 genetic polymorphism (rs17317275) and serum level in rheumatoid arthritis patients infected with CMV. Plant Arch. 2020;20(Suppl 1):582–587.

8. Al Bayati OH, Abood WN, Salloom DF. Detection of Epstein–Barr virus infection in reactive arthritis patients. Iraqi J Sci. 2020;61(10):2479–2485. https://doi.org/10.1128/jb.179.15.4919-4928.1997

9. Ball RJ, Avenell A, Aucott L, et al. Systematic review and meta analysis of the sero epidemiological association between Epstein–Barr virus and rheumatoid arthritis. Arthritis Res Therap. 2015;17:274. https://doi.org/10.1186/s13075-015-0755-6

10. Jonsson A, Hjalmarsson C, Falk P. Levels of matrix metalloproteinases differ in plasma and serum – aspects regarding analysis of biological markers in cancer. Br J Cancer. 2016;115:703–706. https://doi.org/10.1038/bjc.2016.127

11. Sabnis RW. Handbook of biological dyes and stains: synthesis and industrial application. Hoboken (NJ): Wiley; 2010. https://doi.org/10.1002/0471709085

12. Miceli Richard C, Gestermann N, Amiel C, et al. Effect of methotrexate and anti TNF on Epstein–Barr virus T cell response and viral load in patients with rheumatoid arthritis or spondylarthropathies. Arthritis Res Therap. 2009;11(3). https://doi.org/10.1186/ar2708

13. Hamid ZA. The impact of hepatitis B virus and Epstein–Barr virus in pathogenesis of rheumatoid arthritis. Biomed Pharmacol J. 2017;10(3):1495–1501.

14. Jassim NS, Aboud RS, Joda AT. Detection of Epstein–Barr virus capsid antigen (EBV CA) in sera of rheumatoid arthritis, reactive arthritis and ankylosing spondylitis patients. Iraqi J Sci. 2015;56(4B):3130–3134.

15. Jassim NS, Aboud RS, Fadil HY. Detection of Epstein–Barr virus infection in patients with arthritis by immunological and molecular methods. Med J Sulaimani. 2016;27(2). https://doi.org/10.24996/ijs.2020.61.10.4

16. Kuri A, Jacobs BM, Vickaryous N. Epidemiology of Epstein–Barr virus infection and infectious mononucleosis in the United Kingdom. BMC Public Health. 2020;20:912. https://doi.org/10.1186/s12889-020-09049-x.

17. Damania B, Kenney SC, Raab-Traub N. Epstein-Barr virus: Biology and clinical disease. Cell. 2022;185(20):3652-3670. https://doi.org/10.1016/j.cell.2022.08.026.

18. Katz BZ, Shiraishi Y, Mears CJ, Binns HJ, Taylor R. Chronic fatigue syndrome after infectious mononucleosis in adolescents. Pediatrics. 2009;124(1):189-193. https://doi.org/10.1542/peds.2008-1879.

19. Huang W, Bai L, Tang H. Epstein-Barr virus infection: the micro and macro worlds. Virol J, 2023; 20: 220. https://doi.org/10.1186/s12985-023-02187-9.

20. Sausen DG, Bhutta MS, Gallo ES, Dahari H, Borenstein R. Stress-Induced Epstein-Barr Virus Reactivation. Biomolecules. 2021;11(9):1380. https://doi.org/10.3390/biom11091380.

21. Cusick MF, Libbey JE, Fujinami RS. Molecular mimicry as a mechanism of autoimmune disease. Clin Rev Allergy Immunol. 2012;42(1):102-111. https://doi.org/10.1007/s12016-011-8294-7.

22. Ortega-Hernandez O-D, Martínez-Cáceres EM, Presas-Rodríguez S, Ramo-Tello C. Epstein-Barr Virus and Multiple Sclerosis: A Convoluted Interaction and the Opportunity to Unravel Predictive Biomarkers. Int. J. Mol. Sci. 2023;24(8):7407. https://doi.org/10.3390/ijms24087407.

23. Soldan SS, Lieberman PM. Epstein-Barr Virus Infection in the Development of Neurological Disorders. Drug Discov Today Dis Models. 2020;32(Pt A):35-52. https://doi.org/10.1016/j.ddmod.2020.01.001.

24. Thomas OG, Rickinson A, Palendira U. Epstein-Barr virus and multiple sclerosis: moving from questions of association to questions of mechanism. Clin Transl Immunol. 2023;12(5):e1451. https://doi.org/10.1002/cti2.1451.

25. Toussirot E, Roudier J. Epstein–Barr virus in autoimmune diseases. Best Prac Res Clin Rheumatol. 2008;22:883–896. https://doi.org/10.1016/j.berh.2008.09.007.

26. Morawiec N, Adamczyk B, Spyra A, Herba M, Boczek S, Korbel N, Polechoński P, Adamczyk-Sowa M. The Role of Epstein-Barr Virus in the Pathogenesis of Autoimmune Diseases. Medicina. 2025; 61(7):1148. https://doi.org/10.3390/medicina61071148.