Evaluating The Association Between Epstein-Barr Virus And Multiple Sclerosis

Penulis

  • Ankitha G Bhat Department of MLT, Acharya Institute of Allied Health Sciences, Bengaluru, India
  • Nandini P Department of Microbiology, Acharya Institute of Allied Health Sciences, Bengaluru, India

DOI:

https://doi.org/10.58222/juvokes.v3i2.1189

Kata Kunci:

Epstein Barr virus, Multiple Sclerosis, neurodegenerative disorders, immunological changes.

Abstrak

The highly contagious human herpes virus Epstein-Barr Virus (EBV) affects almost every person at some point in their lifetime. Seroconversion—the production of antibodies—occurs primarily in the early years of life, although it can also happen in adolescence or later in life as a result of EBV infection and the immunological response that goes along with it. Adolescents who contract infectious mononucleosis may experience extensive lymphocytosis, an acute, dangerous illness. Although semen or blood are rarely used in the transmission of EBV, saliva is the primary medium. Strong epidemiological and molecular evidence has been presented in recent research investigations supporting the causal role of EBV in multiple sclerosis (MS). MS is the most common chronic inflammatory and neurodegenerative illness of the central nervous system. It is believed that an infectious agent, primarily Epstein-Barr virus, causes the disease in genetically predisposed individuals. It is unclear how a common virus that usually causes benign latent infections might exacerbate autoimmune diseases and cancer in groups that are already at risk. Here, we summarise the data supporting EBV's role as a causative agent for MS and discuss how different risk variables could impact immunological regulation and EBV infection.

Referensi

Rostgaard K, Balfour HHJr, Jarrett R, Erikstrup C, Pedersen O, Ullum H, et al. Primary Epstein-Barr virus infection with and without infectious mononucleosis. PLoS One (2019) 12:e0226436. doi: 10.1371/ journal.pone.0226436

Dunmire SK, Hogquist KA, Balfour HH. Infectious Mononucleosis. Curr Top Microbiol Immunol (2015) 390:211. doi: 10.1007/978-3-319-22822-8_9

Dunmire SK, Verghese PS, Balfour HHJr. Primary Epstein-Barr virus infection. J Clin Virol (2018) 102:84. doi: 10.1016/j.jcv.2018.03.001

Chan KH, Tam JS, Peiris JS, Seto WH, Ng MH. Epstein-Barr virus (EBV) infection in infancy. J Clin Virol (2001) 1:57. doi: 10.1016/s1386-6532(01) 00149-4

Epstein MA, Achong BG, Barr YM. Virus particles in cultured lymphoblasts from Burkitt’s lymphoma. Lancet (1964) 7335:702. doi: 10.1016/s0140-6736 (64)91524-7

Majerciak V, Yang W, Zheng J, Zhu J, Zheng ZM. A Genome-Wide Epstein Barr Virus Polyadenylation Map and Its Antisense RNA to EBNA. J Virol (2019) 2:e01593. doi: 10.1128/JVI.01593-18

Sakamoto K, Sekizuka T, Uehara T, Hishima T, Mine S, Fukumoto H, et al. Next- generation sequencing of miRNAs in clinical samples of Epstein-Barr virus- associated B-cell lymphomas. Cancer Med (2017) 3:605. doi: 10.1002/cam4.1006

Tarbouriech N, Buisson M, Geoui T, Daenke S, Cusack S, Burmeister WP. Structural genomics of the Epstein-Barr virus. Acta Crystallogr D Biol Crystallogr (2006) 10:1276. doi: 10.1107/S0907444906030034

Longnecker R, Neipel F. Introduction to the human g-herpesviruses. In: Arvin A, Campadelli-Fiume G, Mocarski E, Moore PS, Roizman B, Whitley R, et al. editors. Human Herpesviruses. Cambridge, UK: Cambridge University Press (2007). p. 341– 59.

Delecluse S, Poirey R, Zeier M, Schnitzler P, Behrends U, Tsai MH, et al. Identification and Cloning of a New Western Epstein-Barr Virus Strain That Efficiently Replicates in Primary B Cells. J Virol (2020) 94:e01918. doi: 10.1128/JVI.01918-19

Smith NA, Baresel PC, Jackson CL, Ogolla S, Toko EN, Heit S, et al. Differences in the Epstein-Barr Virus gp350 IgA Antibody Response Are Associated With Increased Risk for Coinfection With a Second Strain of Epstein-Barr Virus. J Infect Dis (2019) 6:955. doi: 10.1093/infdis/jiy601

Liu F, Zhou ZH. Comparative virion structures of human herpesviruses. In: Arvin A, Campadelli-Fiume G, Mocarski E, Moore PS, Roizman B, Whitley R, et al., editors. Human Herpesviruses, Cambridge, UK: Cambridge University Press (2007). p. 27–43.

Buschle A, Hammerschmidt W. Epigenetic lifestyle of Epstein-Barr virus. Semin Immunopathol (2000) 42:131. doi: 10.1007/s00281-020-00792-2

Möhl BS, Chen J, Sathiyamoorthy K, Jardetzky TS, Longnecker R. Structural and Mechanistic Insights into the Tropism of Epstein-Barr Virus. Mol Cells (2016) 4:286. doi: 10.14348/molcells.2016.0066

Hammerschmidt W. The Epigenetic Life Cycle of Epstein-Barr Virus. Curr Top Microbiol Immunol (2015) 390:103. doi: 10.1007/978-3-319-22822-8_6

Hatton OL, Harris-Arnold A, Schaffert S, Krams SM, Martinez OM. The interplay between Epstein-Barr virus and B lymphocytes: implications for infection, immunity, and disease. Immunol Res (2014) 2-3:268. doi: 10.1007/s12026-014-8496-1

Odumade OA, Hogqu KA. Progress and Problems in Understanding and Managing Primary Epstein-Barr Virus Infections. Clin Microbiol Rev (2011) 1:193. doi: 10.1128/CMR.00044-10

Crawford DH. Biology and disease associations of Epstein-Barr virus. Philos Trans R Soc Lond B Biol Sci (2001) 1408:461. doi: 10.1098/rstb.2000.0783

Thorley-Lawson DA, Babcock GJ. A model for persistent infection with Epstein-Barr virus: the stealth virus of human B cells. Life Sci (1999) 65:1433. doi: 10.1016/s0024- 3205(99)00214-3

Möhl BS, Chen J, Park SJ, Jardetzky TS, Longnecker R. Epstein-Barr Virus Fusion with Epithelial Cells Triggered by gB Is Restricted by agL Glycosylation Site. J Virol (2017) 91:e01255. doi: 10.1128/JVI.01255-17

Shannon-Lowe C, Rowe M. Epstein Barr virus entry; kissing and conjugation. Curr Opin Virol (2014) 4:78. doi: 10.1016/j.coviro.2013.12.001

Heldwein EE. gH/gL supercomplexes at early stages of herpesvirus entry. Curr Opin Virol (2016) 18:1. doi: 10.1016/j.coviro.2016.01.010

Chesnokova LS, Hutt-Fletcher LM. Epstein-Barr virus infection mechanisms. Chin J Cancer (2014) 33:545. doi: 10.5732/cjc.014.10168

Zhang H, Li Y, Wang HB, Zhang A, Chen ML, Fang ZX, et al. Ephrin receptor A2 is an epithelial cell receptor for Epstein-Barr virus entry. Nat Microbiol (2018) 3:1. doi: 10.1038/s41564-017-0080-8

Latour S, Fischer A. Signaling pathways involved in the T-cell-mediated immunity against Epstein-Barr virus: Lessons from genetic diseases. Immunol Rev (2019) 1:174. doi: 10.1111/imr.12791

Münz C. Epstein-Barr Virus-Specific Immune Control by Innate Lymphocytes. Front Immunol (2017) 8:1658. doi: 10.3389/fimmu. 2017.01658

Chijioke O, Azzi T, Nadal D, Münz C. Innate immune responses against Epstein Barr virus infection. J Leukoc Biol (2013) 6:1185. doi: 10.1189/ jlb.0313173

Iizasa H, Kim H, Kartika AV, Kanehiro Y, Yoshiyama H. Role of Viral and Host microRNAs in Immune Regulation of Epstein-Barr Virus-Associated Diseases. Front Immunol (2020) 11:367. doi: 10.3389/fimmu.2020.00367

Münz C. Latency and lytic replication in Epstein-Barr virus-associated oncogenesis. Nat Rev Microbiol (2019) 17:691. doi: 10.1038/s41579-019-0249-7

Kempkes B, Robertson ES. Epstein-Barr virus latency: current and futureperspectives. Curr Opin Virol (2015) 14:138. doi: 10.1016/j.coviro.2015.09.007

Liebermann PM, Hu J, Renne R. Maintenance and replication during latency. In: Arvin A, Campadelli-Fiume G, Mocarski E, Moore PS,Roizman B, Whitley R, et al.,editors. Human Herpesviruses. Cambridge, UK: Cambridge University Press (2007).p. 379–402.

Dugan JP, Coleman CB, Haverkos B. Opportunities to Target the Life Cycle of Epstein-Barr Virus (EBV) in EBV-Associated Lymphoproliferative Disorders. Front Oncol (2019) 9:127. doi: 10.3389/fonc.2019.00127

Houldcroft CJ, Kellam P. Host genetics of Epstein-Barr virus infection, latency and disease. Rev Med Virol (2015) 20152:71. doi: 10.1002/rmv.1816

Helminen M, Lahdenpohja N, Hurme M. Polymorphism of the interleukin-10 gene is associated with susceptibility to Epstein-Barr virus infection. J Infect Dis (1999) 180:496. doi: 10.1086/314883

Pender MP. The Essential Role of Epstein-Barr Virus in the Pathogenesis of Multiple Sclerosis. Neuroscientist (2011) 17:351. doi: 10.1177/1073858410381531

Hedström AK, Bonfim IL, Hillert J, Olsson T, Alfredsson L. Obesity interacts with infectious mononucleosis in risk of multiple sclerosis. Eur J Neurol (2015) 22:578. doi: 10.1111/ene.12620

Kasifoglu N, Oz S, Dinleyici EC, Us T, Bor O, Durmaz G, et al. Comparison of Methods Used for the Diagnosis of Epstein-Barr Virus Infections in Children. Pol J Microbiol (2018) 1:81. doi: 10.5604/01.3001.0010.6287

Lam WKJ, Jiang P, Chan KCA, Cheng SH, Zhang H, Peng W, et al. Sequencing- based counting and size profiling of plasma Epstein-Barr virus DNA enhance population screening of nasopharyngeal carcinoma. Proc Natl Acad Sci U S A (2018) 22:E5115. doi: 10.1073/pnas.1804184115

Cao P, Zhang M, Wang W, Dai Y, Sai B, Sun J, et al. Fluorescence in situ hybridization is superior for monitoring Epstein Barr viral load in infectious mononucleosis patients. BMC Infect Dis (2017) 1:323. doi: 10.1186/s12879-017- 2412-y

Joshi, N., Usuku, K. & Hauser, S. L. The T-cell response to myelin basic protein in familial multiple sclerosis:diversity of fine specificity, restricting elements, and T-cell receptor usage. Ann. Neurol. 34, 385–393 (1993).

Martin, C. et al. Absence of seven human herpesviruses, including HHV-6, by polymerase chain reaction in CSF and blood from patients with multiple sclerosis and optic neuritis. Acta Neurol. Scand. 95, 280–283 (1997).

Lisak, R. P. et al. B cells from patients with multiple sclerosis induce cell death via apoptosis in neurons in vitro. J. Neuroimmunol. 309, 88–99 (2017).

Li, R. et al. Proinflammatory GM-CSF-producing B cells in multiple sclerosis and B cell depletion therapy. Sci. Transl. Med. 7, 310ra166 (2015).

van Nierop, G. P., Mautner, J., Mitterreiter, J. G., Hintzen, R. Q. & Verjans, G. M. Intrathecal CD8 T-cells of multiple sclerosis patients recognize lytic Epstein-Barr virus proteins. Mult. Scler. 22, 279–291 (2016).

Virtanen, J. O., Wohler, J., Fenton, K., Reich, D. S. & Jacobson, S. Oligoclonal bands in multiple sclerosis reactive against two herpesviruses and association with magnetic resonance imaging findings. Mult. Scler. 20, 27–34 (2014).

Franciotta, D. et al. Cerebrospinal BAFF and Epstein-Barr virus-specific oligoclonal bands in multiple sclerosis and other inflammatory demyelinating neurological diseases. J. Neuroimmunol. 230, 160–163 (2011).

Cagol, A. et al. Association of brain atrophy with disease progression independent of relapse activity in patients with relapsing multiple sclerosis. JAMA Neurol. https://doi.org/10.1001/jamaneurol.2022. 1025 (2022).

Kim, W. & Patsopoulos, N. A. Genetics and functional genomics of multiple sclerosis.Semin. Immunopathol. 4, 63–79 (2022).

Hue SS, Oon ML, Wang S, Tan SY, Ng SB. Epstein-Barr virus-associated T and NK- cell lymphoproliferative diseases: an update and diagnostic approach. Pathology (2020) 1:111. doi: 10.1016/j.pathol.2019.09.011

Iwatsuki K, Miyake T, Hirai Y, Yamamoto T. Hydroa vacciniforme: a distinctive form of Epstein-Barr virus-associated T-cell lymphoproliferative disorders. Eur J Dermatol (2019) 1:21. doi: 10.1684/ejd.2018.3490

Robinson WH, Younis S, Love ZZ, Steinman L, Lanz TV. Epstein-Barr virus as a potentiator of autoimmune diseases. Nat Rev Rheumatol. 2024 Oct 10. doi: 10.1038/s41584-024-01167-9. Epub ahead of print. PMID: 393902

Unduhan

Diterbitkan

2024-12-31

Terbitan

Bagian

Articles

Cara Mengutip

Evaluating The Association Between Epstein-Barr Virus And Multiple Sclerosis. (2024). Jurnal Vokasi Kesehatan, 3(2), 133-140. https://doi.org/10.58222/juvokes.v3i2.1189

Artikel Serupa

Anda juga bisa Mulai pencarian similarity tingkat lanjut untuk artikel ini.