The interaction between Epstein–Barr virus and multiple sclerosis genetic risk loci: insights into disease pathogenesis and therapeutic opportunities
Abstract Multiple sclerosis (MS) is a chronic neurodegenerative autoimmune disease, characterised by the demyelination of neurons in the central nervous system. Whilst it is unclear what precisely leads to MS, it is believed that genetic predisposition combined with environmental factors plays a piv...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2023-01-01
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| Series: | Clinical & Translational Immunology |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/cti2.1454 |
| _version_ | 1797780768287621120 |
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| author | Ali Afrasiabi Chantelle Ahlenstiel Sanjay Swaminathan Grant P Parnell |
| author_facet | Ali Afrasiabi Chantelle Ahlenstiel Sanjay Swaminathan Grant P Parnell |
| author_sort | Ali Afrasiabi |
| collection | DOAJ |
| description | Abstract Multiple sclerosis (MS) is a chronic neurodegenerative autoimmune disease, characterised by the demyelination of neurons in the central nervous system. Whilst it is unclear what precisely leads to MS, it is believed that genetic predisposition combined with environmental factors plays a pivotal role. It is estimated that close to half the disease risk is determined by genetic factors. However, the risk of developing MS cannot be attributed to genetic factors alone, and environmental factors are likely to play a significant role by themselves or in concert with host genetics. Epstein–Barr virus (EBV) infection is the strongest known environmental risk factor for MS. There has been increasing evidence that leaves little doubt that EBV is necessary, but not sufficient, for developing MS. One plausible explanation is EBV may alter the host immune response in the presence of MS risk alleles and this contributes to the pathogenesis of MS. In this review, we discuss recent findings regarding how EBV infection may contribute to MS pathogenesis via interactions with genetic risk loci and discuss possible therapeutic interventions. |
| first_indexed | 2024-03-12T23:48:31Z |
| format | Article |
| id | doaj.art-90bf01d7599b49fb89161bce59747d7a |
| institution | Directory Open Access Journal |
| issn | 2050-0068 |
| language | English |
| last_indexed | 2024-03-12T23:48:31Z |
| publishDate | 2023-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Clinical & Translational Immunology |
| spelling | doaj.art-90bf01d7599b49fb89161bce59747d7a2023-07-14T02:50:29ZengWileyClinical & Translational Immunology2050-00682023-01-01126n/an/a10.1002/cti2.1454The interaction between Epstein–Barr virus and multiple sclerosis genetic risk loci: insights into disease pathogenesis and therapeutic opportunitiesAli Afrasiabi0Chantelle Ahlenstiel1Sanjay Swaminathan2Grant P Parnell3EBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research University of Sydney Sydney NSW AustraliaKirby Institute University of New South Wales Sydney NSW AustraliaEBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research University of Sydney Sydney NSW AustraliaEBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research University of Sydney Sydney NSW AustraliaAbstract Multiple sclerosis (MS) is a chronic neurodegenerative autoimmune disease, characterised by the demyelination of neurons in the central nervous system. Whilst it is unclear what precisely leads to MS, it is believed that genetic predisposition combined with environmental factors plays a pivotal role. It is estimated that close to half the disease risk is determined by genetic factors. However, the risk of developing MS cannot be attributed to genetic factors alone, and environmental factors are likely to play a significant role by themselves or in concert with host genetics. Epstein–Barr virus (EBV) infection is the strongest known environmental risk factor for MS. There has been increasing evidence that leaves little doubt that EBV is necessary, but not sufficient, for developing MS. One plausible explanation is EBV may alter the host immune response in the presence of MS risk alleles and this contributes to the pathogenesis of MS. In this review, we discuss recent findings regarding how EBV infection may contribute to MS pathogenesis via interactions with genetic risk loci and discuss possible therapeutic interventions.https://doi.org/10.1002/cti2.1454EBNA2EBVGWASmultiple sclerosisrisk genetic variationRNA therapeutics targeting EBV |
| spellingShingle | Ali Afrasiabi Chantelle Ahlenstiel Sanjay Swaminathan Grant P Parnell The interaction between Epstein–Barr virus and multiple sclerosis genetic risk loci: insights into disease pathogenesis and therapeutic opportunities Clinical & Translational Immunology EBNA2 EBV GWAS multiple sclerosis risk genetic variation RNA therapeutics targeting EBV |
| title | The interaction between Epstein–Barr virus and multiple sclerosis genetic risk loci: insights into disease pathogenesis and therapeutic opportunities |
| title_full | The interaction between Epstein–Barr virus and multiple sclerosis genetic risk loci: insights into disease pathogenesis and therapeutic opportunities |
| title_fullStr | The interaction between Epstein–Barr virus and multiple sclerosis genetic risk loci: insights into disease pathogenesis and therapeutic opportunities |
| title_full_unstemmed | The interaction between Epstein–Barr virus and multiple sclerosis genetic risk loci: insights into disease pathogenesis and therapeutic opportunities |
| title_short | The interaction between Epstein–Barr virus and multiple sclerosis genetic risk loci: insights into disease pathogenesis and therapeutic opportunities |
| title_sort | interaction between epstein barr virus and multiple sclerosis genetic risk loci insights into disease pathogenesis and therapeutic opportunities |
| topic | EBNA2 EBV GWAS multiple sclerosis risk genetic variation RNA therapeutics targeting EBV |
| url | https://doi.org/10.1002/cti2.1454 |
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